NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)

CEREBRAL PALSY (CP)

COLLADO, DIANA NICOLE D.
MR. ALLAN PAULO BLAQUERA, RN
TOPIC OUTLINE
Neurological System • Hypo and Hypernatremia
• Cerebral Palsy • Hypo and Hyperkalemia
• Seizure Disorder
Immune System
• Autism Spectrum Disorder (ASD)
• Allergies
• Amyotrophic Lateral Sclerosis (ALS)
• Dengue
• Tourette’s Syndrome
• Streptococcal Infections
Endocrine System
• Type 1 Diabetes Mellitus Cellular Aberrations
• Leukemias
Fluid and Electrolyte Imbalances
• Fluid Volume Renal System
• Hypo and Hypervolemia • Urinary Tract Infection (UTI)
• Acute Glomerulonephritis (AGN)

ATTENDANCE: SCHEDULE:
BUENAVENTURA, NIÑO KAE C. 01/10 (STUDY OWN TOPIC & MAKE OUTLINE)
CALATI, KELLY KEITH JANN R.
01/12 (FIRST SGL)
CALIGUIRAN, MARIA ERIKA C.
CASTILLO, MICHELLE T. 01/12 (FINALIZATION OF HYPOTHESIS)
COLLADO, DIANA NICOLE D. 01/12 (PATHOPHYSIOLOGY MAKING)
CORTEZ, ELLYZA L. 01/13 (NCP MAKING)
DAYAG, CEE JAR MARIE G. 01/15 (FINALIZATION OF PATHOPHYSIOLOGY AND NCP)
FABELLAR, AIDON JOSH B. 01/20 (PLENARY FOR SCENARIO 6)
GADDAO, CRISTIAN REY I.

CEREBRAL PALSY (CP)

– Group of nonprogressive disorders of upper motor Other symptoms:
neuron impairment that result in motor dysfunction. • Feeding, drooling and swallowing difficulties
– Affected children also may have speech or ocular • Constipation
difficulties, seizures, cognitive challenges, or • Problems with speaking and communication
hyperactivity. Muscle spasticity can lead to orthopedic • Seizures or fits (epilepsy)
or gait difficulties • Difficulty falling asleep and/or staying asleep
– Most frequently in very-low-birth-weight infants and • Gastroesophageal reflux disease (GERD) – where
those who are small for gestational age; it is increasing acid from the stomach leaks up into the esophagus
in incidence because of the number of very-low-birth- (gullet)
weight infants who survive today • An abnormally curved spine (scoliosis)
• Hips that pop out (dislocate) easily
CAUSE:
• Difficulty controlling the bladder (urinary incontinence)
• CP is caused by abnormal brain development or
• A learning disability
damage to the developing brain, leading to cell
destruction of the motor tracts. • Eye problems – including reduced visions, a squint, or
uncontrollable eye movements
• Nutritional deficiencies, drug use, and maternal
infections such as cytomegalovirus or toxoplasmosis, • Hearing loss
as well as direct birth injury, may also contribute to
the cause. CAUSE
• Infections such as meningitis or encephalitis can
PROBLEMS BEFORE BIRTH
result in CP symptoms as well.
• Damage to the part of the brain called white matter,
SIGNS AND SYMPTOMS possible as a result of a reduced blood or oxygen
The main symptoms of cerebral palsy are problems with supply (periventricular leukomalacia [PVL])
movements, coordination, and development. • An infection caught by the mother – such as
cytomegalovirus, rubella, chickenpox, or
Possible signs in a child include: toxoplasmosis
• Delays in reaching development milestone – for • A stroke – where there’s bleeding in the baby’s brain
example, not sitting by 8 months or not walking by 18 or the blood supply to their brain is cut off
months • An injury to the unborn baby’s head
• Seeming too stiff or too floppy (hypotonia)
• Weak arms or legs PROBLEMS DURING OR AFTER BIRTH
• Fidgety, jerky, or clumsy movements • The brain temporarily not getting enough oxygen
• Random, uncontrolled movements (asphyxiation) during a difficult birth
• Muscle spasms • An infection of the brain, such as meningitis
• Shaking hands (tremors) • A serious head injury
• Walking on tiptoes • Choking or nearly drowning, resulting in the brain not
getting enough oxygen
The parts of the body affected can also vary. Sometimes • A very low blood sugar level
only one side of the body is affected, sometimes the whole • A stroke
body is affected, and sometimes mainly the legs are
affected.
INCREASED RISK
• being born prematurely (before the 37th week of
pregnancy) – babies born at 32 weeks or earlier are at D. MIXED TYPE
a particularly high risk – Some children show symptoms of both spasticity and
• having a low birthweight athetoid or ataxic and athetoid movements.
• being part of a multiple birth, such as a twin or triplet – This combination obviously results in a severe degree
• the mother smoking, drinking a lot of alcohol, or taking of physical impairment.
drugs such as cocaine, during pregnancy
ASSESSMENT
TYPES OF CEREBRAL PALSY • The diagnosis of CP is based on history and physical
assessment.
A. SPATIC TYPE o Any episode of possible anoxia during prenatal
– Spasticity is excessive tone in the voluntary muscles life or at birth should be documented.
that results from loss of upper motor neurons. • Children with all forms of CP may have sensory
– A child with spastic CP has hypertonic muscles, alterations such as:
abnormal clonus, exaggeration of deep tendon reflexes, o strabismus
abnormal reflexes such as a positive Babinski reflex, o refractive disorders
and continuation of neonatal reflexes, such as the tonic o visual perception problems
neck reflex, well past the age at which these usually o visual field defects
disappear. o speech disorders such as abnormal rhythm or
– If infants with CP are held in a ventral suspension articulation.
position, they arch their backs and extend their arms
and legs abnormally. • They may show an attention deficit disorder or autism
– Children with CP fail to demonstrate a parachute reflex spectrum syndrome.
if lowered suddenly and tend to assume a “scissors • Cognitive challenge and recurrent seizures also
gait” because tight adductor thigh muscles cause their frequently accompany all types of the disorder.
legs to cross when held upright. This involvement may • A skull X-ray or ultrasound may show cerebral
be so severe that it leads to a subluxated hip. asymmetry.
• An EEG may be abnormal, although the pattern is
Spastic involvement may affect: highly variable.
• Hemiplegia – Both extremities on one side
o Children with hemiplegia usually have greater
involvement in the arm than the leg. The
involved arm may be shorter and may have a
smaller muscle circumference than the other
arm. Most children with hemiplegia have
difficulty identifying objects placed in their
involved hand when their eyes are closed
(astereognosis).

• Quadriplegia – all four extremities

o A child with quadriplegia invariably has impaired
speech (pseudobulbar palsy) but may or may
not be cognitively challenged. Swallowing saliva
may be so difficult that the child drools and has
difficulty swallowing food

• Diplegia or paraplegia – primarily the lower

extremities

B. DYSKINETIC OR ATHETOID TYPE

– The athetoid type of CP involves abnormal involuntary
movement (athetoid means “wormlike”).
o Early in life, the child appears limp and flaccid.
o Later, in place of voluntary movement, children
make slow, writhing motions.
o This can involve all four extremities plus the
face, neck, and tongue. Because of the poor
tongue and swallowing movements, the child
drools and speech are difficult to understand.
o Under emotional stress, the involuntary
movements may become irregular and jerking
(choreoid) with disordered muscle tone
(dyskinetic).

C. ATAXIC TYPE
– Children with ataxic involvement have an awkward,
wide-based gait.
– On neurologic examination, they are unable to perform
fine coordinated motions, the finger-to-nose test, or
rapid, repetitive movements (tests of cerebellar
function).
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
SEIZURE DISORDER
CASTILLO MICHELLE T.
MR. ALLAN PAULO BLAQUERA, RN

SEIZURE DISORDER – If awareness is impaired during any part of the

– A seizure is an abnormal, unregulated electrical seizure, the seizure is classified as a focal impaired-
discharge that occurs within the brain’s cortical gray awareness seizure.
matter and transiently interrupts normal brain function.
– A seizure typically causes altered awareness, abnormal FOCAL AWARE SEIZURES
sensations, focal involuntary movements or • The person is aware and may experience feelings
convulsions. such as déjà vu, an unpleasant smell or taste, or
sensation such as ‘butterflied’ or nausea
DEFINITIONS AND TERMINOLOGY TO SEIZURES: • These seizures may also involve motor activity (such
as involuntary and brief jerking of an arm or leg) or
EPILEPSY autonomic behaviors (such as fiddling with clothing
– Also called epileptic seizures disorder or pointing)
– A chronic brain disorder characterized by recurrent (>2)
seizures that are unproveked (ie, , not related to
reversible stressors) and that occur > 24 hours apart. FOCAL IMPAIRED AWARENESS SEIZURES
– A single seizure is not considered an epileptic seizure. • During these seizures the person may appear
Epilepsy is often idiopathic, but various brain confused and dazed
disorders, such as malformations, strokes, and • Strange and repetitive actions (such as fiddling with
tumors, can cause symptomatic epilepsy. their clothes, making chewing movements with their
mouth or uttering unusual sounds)
SYMPTOMATIC EPILEPSY • Used to be called complex partial seizures
– Is epilepsy due to a known cause (eg, brain tumor,
stroke. Focal-onset motor seizures may be further classified by
– The seizures it causes are called symptomatic type of seizure:
epileptic seizures. Such seizures are most common • Automatisms (coordinated, purposeless, repetitive
among neonates and older people. motor activity)
• Atonic (focal loss of muscle tone)
CRYPTOGENIC EPILEPSY • Clonic (focal rhythmic jerking)
– is epilepsy assumed to be due to a specific cause, but
• Epileptic spasms (focal flexion or extension of arms
whose specific cause is currently unknown.
and flexion of trunk)
– cryptogenic epilepsy and often in refractory epilepsy,
a rare but increasingly identified cause is anti-NMDA • Hyperkinetic (causing pedaling or thrashing)
(N-methyl-d-aspartate) receptor encephalitis, • Myoclonic (irregular, brief focal jerking)
especially in young women • Tonic (sustained focal stiffening of one limb or one
– This disorder also causes psychiatric symptoms, a side of the body)
movement disorder, and cerebrospinal fluid (CSF)
pleocytosis. Awareness level is usually not specified for atonic seizures
or epileptic spasms.
NONEPILEPTIC SEIZURES
– are provoked by a temporary disorder or stressor (eg, In focal-onset tonic seizures, stiffening involves only one
metabolic disorders, central nervous system (CNS) limb or one side of the body, usually with no loss of
infections, cardiovascular disorders, drug toxicity por consciousness. electroencephalography (EEG) may show
withdrawal, psychogenic disorders). contralateral focal epileptiform abnormalities. In contrast, in
– In children, fever can provoke a seizure (febrile generalized-onset tonic seizures, stiffening involves all
seizures). limbs, with or without loss of consciousness, and EEG may
show bilateral epileptiform abnormalities.
PSYCHOGENIC NONEPILEPTIC SEIZURES
– are symptoms that simulate seizures in patients with Focal-onset nonmotor seizures may be further classified
psychiatric disorders but that do not involve an based on the earliest prominent feature:
abnormal electrical discharge in the brain. • Autonomic dysfunction (autonomic effects such as
gastrointestinal (GI) sensations, a sense of heat or
DIFFERENT SEIZURE DISORDERS cold, flushing, sexual arousal, piloerection, and
palpitations)
A. FOCAL ONSET SEIZURES
– Focal-onset seizures originate in networks in one • Behavior arrest (cessation of movement and
hemisphere and may originate in subcortical unresponsiveness as the main feature of the entire
structures. seizure)
– They may be discretely localized or more widely • Cognitive dysfunction (impairment of language or
distributed. other cognitive domains or positive features such as
– Focal seizures are described on the basis of their déjà vu, hallucinations, illusions, or perceptual
onset (motor or non-motor) and whether or not the distortions)
person is aware during the seizure • Emotional dysfunction (manifesting with emotional
– Focal-onset seizures may be classified by level of changes, such as anxiety, fear, joy, other emotions,
awareness: or affective signs without subjective emotions)
• Focal aware seizures (formerly, simple partial • Sensory dysfunction (causing somatosensory,
seizures) olfactory, visual, auditory, gustatory, or vestibular
• Focal impaired-awareness seizures (formerly, sensations or a sense of heat or cold)
complex partial seizures)
Focal-onset seizures may evolve into a generalized-onset • A sequence of a brief tonic episode followed by an
tonic-clonic seizure (called a focal-to-bilateral tonic-clonic atonic seizure is called tonic-atonic seizure
seizure; formerly, secondary generalization), which causes
loss of consciousness. Focal-to-bilateral tonic-clonic UNKNOWN-ONSET SEIZURES
seizures occur when a focal-onset seizure spreads and – Seizures are usually classified as unknown-onset
activates the entire cerebrum bilaterally. Activation may seizures when information about onset is lacking.
occur so rapidly that the initial focal-onset seizure is not – If clinicians acquire more information about the
clinically apparent or is very brief. seizures, these seizures may be reclassified as focal-
onset or generalized-onset.
B. GENERALIZED ONSET SEIZURES – Seizures of unknown onset can be motor or nonmotor.
• This seizure are surges of abnormal nerve discharges – Unknown-onset motor seizures may be further
throughout the cortex of the brain more or less at the classified as:
same time • Tonic-clonic
• The most common cause is an imbalance in the • Epileptic spasms
“brakes” (inhibitory circuits) and “accelerator” • Behavior arrest
(excitatory circuits) of electrical activity of the brain
• Sleep deprivation or drinking large amounts or alcohol TONIC-CLONIC SEIZURES
can increase the excitatory response and increase the – Tonic-clonic seizures with an obscure onset are often
risk of generalized-onset seizures, especially in classified as unknown-onset seizures.
people with a genetic tendency to have them – Tonic-clonic seizures both involve both tonic
(stiffening) and clonic (twitching or jerking) phase of
ABSENCE SEIZURES (“PETIT MAL SEIZURES”) muscle activity
• Childhood absence epilepsy shows up as brief – They may start with a simple partial seizure or aura.
staring episodes in children (4 to 6 years old) – Two stages: a tonic phase and a clonic phase
• Children usually outgrow these
• Juvenile absence epilepsy starts slightly later and SYMPTOMS OF A TONIC-CLONIC SEIZURE
can persist into adulthood • AURA
• People with these kind of seizures may develop tonic- o It may start with a simple or complex partial
clonic seizures in addition to absence of seizures in seizure known as an aura
adulthood o The person may experience abnormal
sensations such as a particular smell, vertigo,
o consist of 10- to 30-second loss of consciousness with nausea, or anxiety
eyelid fluttering; axial muscle tone may or may not be
lost. • TONIC ACTIVITY
o Patients do not fall or convulse; they abruptly stop o When the tonic-clonic seizure begins, the person
activity, then just as abruptly resume it, with no postictal loses consciousness and may fall
symptoms or knowledge that a seizure has occurred. o Strong tonic spasms of the muscles can force air
o Absence seizures are genetic and occur predominantly out of the lungs, resulting in a cry or moan, even
in children. though the person is not aware of their
surroundings.
MYOCLONIC SEIZURES o There may saliva or foam coming from the mouth
• This consist of sudden body of limb jerks that can o If the person inadvertently bites their tongue or
involve the arms, head, and neck cheek, blood may be visible in the saliva
• The spasms occur on both sides of the body in o Stiffness of the chest muscles may impair
clusters, especially in the morning breathing, the person’s face may look bluish or
• When these seizures develop in adolescence along gray, he or she may make gasping or gurgling
with tonic-clonic seizures, they are part of a syndrome sounds
called juvenile myoclonic epilepsy
• CLONIC ACTIVITY
o The arms and shoulders jerk rhythmically (3 o Jerking movements affect the face, arms, and
times/second), causing progressive lifting of the arms. legs, becoming intense and rapid
o Typically, these seizures last 10 to 60 seconds. o After one to three minutes, the jerking
Impairment of awareness may not be obvious. movements slow down and the body relaxes,
o Myoclonic absence seizures are caused by various something including the bowel or bladder.
genetic disorders; sometimes the cause is unknown. o The person may let out a deep sigh and return to
more normal breathing.
TONIC AND ATONIC SEIZURES (“DROP ATTACKS”)
• AFTER THE SEIZURE (POSTICTAL PERIOD)
• People with multiple brain injuries and intellectual
o After a seizure, the person may remain
disability, have tonic seizures consisting of sudden
unconscious for several minutes as the brain
stiffness in the arms and body, which can cause falls
recovers from the seizure activity. He or she may
and injuries
appear to be sleeping or snoring
• Many persons with tonic seizures have a syndrome
o Gradually the person regains awareness and
called Lennox Gastaut syndrome
may feel confused, exhausted, physically sore,
o It may involve intellectual disability, multiple
sad or embarrassed for a few hours. The person
seizure types including tonic seizures
may not remember having a seizure, and may
o Severe form of epilepsy that causes several
have other memory loss.
types of seizures
o Occasionally, people may have abnormal or
• Persons with diffuse brain disorders also may have combative behavior after a tonic-clonic seizure
atonic seizures, characterized by a sudden loss of while the brain is recovering.
body tone that results in collapsing, often with injuries
NURSING MANAGEMENT DURING A SEIZURE
• Protect the person from injury by helping them to the
floor and clearing away furniture or other items. Do
not attempt to hold the person still
• Do not put anything in the person’s mouth. Putting
things in the mouth may lead to injury
• Time the seizure
• Turn head to side during a seizure activity
• Loosen clothing from neck or chest and abdominal
areas
• A seizure lasting more than 5 minutes is an
emergency
• Calm reassurance can be helpful to a person who is
recovering from a seizure

DIAGNOSIS OF SEIZURE DISORDERS

• Clinical Evaluation
• For new-onset seizures, neuroimaging, laboratory
testing and usually EEG
• For known seizures disorders, usually antiseizure drug
levels
• For new-onset or known seizures disorders, other
testing as clinical indicated.

DIAGNOSTIC TESTS
o Neuroimaging (typically head CT, but sometimes
MRI) is usually done immediately to exclude a mass
or hemorrhage.
o Follow-up MRI is recommended when CT is
negative. It provides better resolution of brain
tumors and abscesses and can detect cortical
dysplasias, cerebral venous thrombosis, and herpes
encephalitis.
o Electroencephalography (EEG) is critical in the
diagnosis of epileptic seizures, particularly of focal
impaired-awareness seizures or absence status
epilepticus, when EEG may be the most definitive
indication of a seizure.
o Inpatient combined video-EEG
monitoring, usually for 2 to 7 days, records EEG
activity and clinical behavior simultaneously. It is the
most sensitive EEG testing available and is thus
useful in differentiating epileptic from nonepileptic
seizures.
o Ambulatory EEG can be done while patients are at
home. It may be useful if seizures recur in patients
who cannot be admitted to the hospital for a long
time.

TREATMENT OF SEIZURE DISORDERS

• Elimination of the cause if possible
• Avoidance of or precautions during situations when
loss of consciousness could be life threatening
• Drugs to control seizures
• Surgery if ≥ 2 drugs in therapeutic doses do not
control seizures
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
AUTISM SPECTRUM DISORDER (ASD)
CORTEZ, ELLYZA L.
MR. ALLAN PAULO BLAQUERA, RN

AUTISM SPECTRUM DISORDER eye contact, and unusual play, with repetitive play and
preference becoming more apparent as the child ages.
– The impairment in communication includes both verbal
and nonverbal skills, and communication may be totally
absent. For children with ASD who do speak, deficiencies
in grammatical structure, an inability to name objects
(nominal aphasia), and abnormal speech melody, such
as question-like rises at the end of statements, may exist.
Echolalia (repetition of words or phrases spoken by
others) and concrete interpretation are also common
findings. Nonverbal deficiencies include abnormal eye
contact, poor use and understanding of body movements
and gestures, and lack of facial expressions.
– Bizarre responses to the environment may include
intense reactions to minor changes in the environment
(perhaps screaming if a toy box is moved across the
room), attachment to odd objects such as always carrying
a string or a shoe, and a rigid demand for routine. For
children with ASD, a minor disruption in their day, such as
having a substitute teacher, may cause a physical or
emotional breakdown
– Autism spectrum disorder (ASD) is a complex range of – Signs in children prior to school age include repetitive
neurodevelopment disorders marked by difficulties in hand movements (clapping or flapping) and constant
three main areas: social deficits, communications body rocking; in these cases, early assessment is
issues, and restricted behaviors, with onset in the early advised. It may be difficult to gain the child’s attention as
developmental stages, that impair everyday functioning. the child becomes intensely preoccupied by music or
Autism is highly variable – the word ‘spectrum’ refers to objects that revolve, such as a fan, the swirling water in
how autism is experienced differently by different people. the toilet bowl, or a spinning top. Aggressive actions, such
– Autism is considered a spectrum because it’s different for as hitting, head banging, and biting, or the inability to feel
every autistic person – some autistic people might need pain, may also be present.
more support than others to live the lives they want to – Children are said to have a labile mood (crying occurs
lead. For example, some people with ASD may have suddenly and is followed immediately by giggling or
advanced conversation skills whereas others may be laughing or vice versa). They may overrespond to
nonverbal. Some people with ASD need a lot of help in sensory stimuli, such as light or sound, but then be
their daily lives; others can work and live with little to no unaware of a major event in the room, such as the sound
support. of a fire alarm.
– ASD occurs in all ethnic and socioeconomic groups, as – In contrast to these mannerisms, long-term memory and
frequently as 1 in 88 children, and more frequently in boys “savant” skills (exceptional skills such as virtuoso piano
than in girls. playing) may be excellent. For example, children with
ASD may be able to recall dates and spoken words from
RISK FACTORS conversations that took place years before. This excellent
• Genetics memory previously led to the belief that most of these
• Advanced parent age children have usual intelligence, but around 50% of
children with ASDs have an intellectual disability as well.
• Rapid succession pregnancies (less than 1 year apart)
• Perinatal complications of pregnancy or birth
COMMON COMMORBIDITIES IN ASD
(Prematurity, Low birth weight, Multiple gestation)
• Intellectual Disability
CLINICAL MANIFESTATIONS • Language Disorders
– Common symptoms in the child with ASD includes: • Anxiety, Depression, Obsessive Compulsive Disorder
• Failure to develop social relations (OCD)
• Stereotyped behaviors such as hand gestures • Symptoms Of ADHD
• Extreme resistance to change in routine • Self-Injurious Behavior
• Abnormal responses to sensory stimuli • Aggressive Behavior
• Decreased sensitivity to pain • Seizures
• Inappropriate or decreased emotional • Tic Disorders
expressions • Food Selectivity
• Specific, limited intellectual problem-solving • Sleep Difficulties
abilities • GI Disorders
• Stereotyped or repetitive use of language
• Impaired ability to initiate or sustain a DIAGNOSIS
conversation – The first step in diagnosis is early detection, typically by
– ASDs often are typically recognizable in children routine developmental screening provided at routine well
between 12 and 24 months but may be noticed earlier if child checks.
the 3351 condition is more severe (APA, 2013). The first – All children should be screened for developmental
symptoms of ASD noticed by parents are delay in delays and disabilities at:
language development, odd communication, lack of • 9 months
social interest, or unusual interactions, such as avoiding • 18 months
• 24 or 30 months
– In addition, all children should be screened specifically
for ASD at:
• 18 months
• 24 or 30 months
– The second step of diagnosis is a comprehensive
evaluation which typically includes:
• Parent and collateral interviews to assess
developmental course, social history, and current
behavioral concerns
• Formal evaluation of:
® Cognitive / developmental abilities
® Speech and language abilities
® Adaptive and social functioning
® Fine/gross motor and sensory functioning
• Direct observation
• May also include a hearing and vision screening,
genetic testing and other medical diagnostic
studies

THERAPEUTIC MANAGEMENT
ASD is a perplexing condition because of the extreme
variability a child may exhibit.
– Primary treatment for children with ASD includes
educational, compensatory, and behavior
modalities, such as the evidence-based applied
behavior analysis (ABA) treatment based on the
associations between behavior and learning. Treatment
such as ABA is typically very intensive and can involve
the entire family, taking place in the home, at agencies,
at school, or in the community; although treatment is
unique to each child, parental involvement is essential to
facilitate development of self-care skills and process with
therapy.
– No specific medications are approved for the
treatment of ASD; however, medications may be used
to modify troublesome symptoms, such as high energy,
inability to focus, depression, or seizures. Atypical
antipsychotic medications, such as risperidone
(Risperdal) and aripiprazole (Abilify), are approved by
the U.S. Food and Drug Administration (FDA) for
children and teens with ASD. Advantages of these
agents include improving sociability while decreasing
tantrums, aggressive outbursts, and self-injurious
behavior.
– “Off-label” medications may be selected to relieve
significant suffering in persons with ASD in the absence
of significantly large and targeted studies. These
medications include selective serotonin reuptake
inhibitors (SSRIs), α2 agonists, antipsychotics,
mood stabilizers, and selective norepinephrine
reuptake inhibitors (SNRIs). Melatonin is an over-the-
counter medication that may be recommended to reduce
sleep difficulties.
– It is important for nurses to ask at healthcare visits
whether parents are finding time for both care of their
child and themselves because there is a danger that
excessive parental stress can lead to child maltreatment
(Hall & Graff, 2012). Encourage parents of children with
ASD to seek support through organizations in the
community to help support their own mental well-being
and that of their families.
– As children mature, they develop greater awareness of
and attachment to parents and other familiar adults. A
day care program can help promote social awareness.
Some children may eventually reach a point where they
can become passively involved in loosely structured play
groups. A small number of children, typically with higher
levels of functioning, may be able to lead independent
lives, although social ineptness and awkwardness may
continue, especially if accompanied by intellectual
disability.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
AMYOTROPHIC LATERAL SCLEROSIS (ALS)
CALATI, KELLY KEITH JANN R.
MR. ALLAN PAULO BLAQUERA, RN

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

– Amyotrophic lateral sclerosis (ALS) is a rare neurological
disease that primarily affects the nerve cells (neurons) TYPES OF ALS
responsible for controlling voluntary muscle movement
(those muscles we choose to move). SPORADIC ALS (sALS)
o Voluntary muscles produce movements like – Most common form of ALS
chewing, walking, and talking. The disease is – This means the disease seems to occur at random with
progressive, meaning the symptoms get worse no clearly associated risk factors and no family history
over time. Currently, there is no cure for ALS and of the disease. Although family members of people with
no effective treatment to halt or reverse the sporadic ALS are at an increased risk for the disease,
progression of the disease. the overall risk is very low and most will not develop
o It is characterized by progressive degeneration of ALS.
nerve cells in the spinal cord and brain
– ”Amyotrophic” comes from the Greek language. "A" FAMILIAL ALS (fALS)
means no. "Myo" refers to muscle. "Trophic" means – FALS is caused by changes to a gene
nourishment. – Parents pass the faulty gene to their children. If one
o Amyotrophic means "no muscle nourishment,” parent has the gene for ALS, each of their children will
and when a muscle has no nourishment, it have a 50% chance of getting the gene and having the
"atrophies" or wastes away. disease
– ALS belongs to a wider group of disorders known as – The familial form of ALS usually only requires one
motor neuron diseases, which are caused by gradual parent to carry the gene responsible for the disease.
deterioration (degeneration) and death of motor
neurons. SIGNS AND SYMPTOMS
o Motor neurons are nerve cells that extend from Early symptoms include:
the brain to the spinal cord and to muscles • fasciculations (muscle twitches) in the arm, leg,
throughout the body. shoulder, or tongue
o As motor neurons degenerate, they stop sending • muscle cramps
messages to the muscles and the muscles
• tight and stiff muscles (spasticity)
gradually weaken, start to twitch, and waste away
• muscle weakness affecting an arm, a leg, neck or
(atrophy).
diaphragm
o Eventually, the brain loses its ability to initiate and
control voluntary movements. • slurred and nasal speech
– Early symptoms of ALS usually include muscle • difficulty chewing or swallowing
weakness or stiffness. Gradually all voluntary muscles • dropping things
are affected, and individuals lose their strength and the • persistent fatigue
ability to speak, eat, move, and even breathe.
– Most people with ALS die from respiratory failure, usually For many individuals the first sign of ALS may appear in the
within 3 to 5 years from when the symptoms first appear. hand or arm as they experience difficulty with simple tasks
– ALS was once commonly known as Lou Gehrig’s such as buttoning a shirt, writing, or turning a key in a lock. In
disease, following the retirement of the famous other cases, symptoms initially affect one of the legs, and
ballplayer in the 1940s due to the disease. people experience awkwardness when walking or running or
they notice that they are tripping or stumbling more often.
When symptoms begin in the arms or legs, it is referred to as
“limb onset” ALS. Other individuals first notice speech or
swallowing problems, termed “bulbar onset” ALS.

® Regardless of where the symptoms first appear, muscle

weakness and atrophy spread to other parts of the body
as the disease progresses.
® Individuals may develop problems with moving,
swallowing (dysphagia), speaking or forming words
(dysarthria), and breathing (dyspnea).
® Individuals with ALS usually have difficulty swallowing
and chewing food, which makes it hard to eat normally
and increases the risk of choking. They also burn
calories at a faster rate than most people without ALS.
® Due to these factors, people with ALS tend to lose weight
rapidly and can become malnourished.
o Because people with ALS usually retain their
ability to perform higher mental processes such
POTENTIAL RISK FACTORS FOR ALS as reasoning, remembering, understanding, and
• Age. Although the disease can strike at any age, problem solving, they are aware of their
symptoms most commonly develop between the ages of progressive loss of function and may become
55 and 75. anxious and depressed.
• Gender. Men are slightly more likely than women to ® Individuals with ALS will have difficulty breathing as the
develop ALS. However, as we age, the difference muscles of the respiratory system weaken. They
between men and women disappears. eventually lose the ability to breathe on their own and
• Race and ethnicity. Most likely to develop the disease must depend on a ventilation
are Caucasians and non-Hispanics.
® Affected individuals also face an increased risk of infection or other problems. CSF is the fluid that
pneumonia during later stages of the disease. Besides bathes the brain and spinal cord.
muscle cramps that may cause discomfort, some
individuals with ALS may develop painful neuropathy • X-ray. This test uses invisible electromagnetic
(nerve disease or damage). energy beams to produce images of internal
tissues, bones, and organs onto film.
CAUSE OF ALS • Magnetic resonance imaging (MRI). This
• Researchers still don't know exactly what causes motor procedure uses large magnets, radiofrequencies,
neurons to die with ALS. Gene changes, or mutations, and a computer to produce detailed images of
are behind 5% to 10% of ALS cases. More than 12 organs and structures within the body.
different gene changes have been linked to ALS. • Electrodiagnostic tests, such as
• One change is to a gene that makes a protein called electromyography (EMG) and nerve conduction
SOD1. This protein may be toxic to motor neurons. study (NCS). These studies evaluate and diagnose
Other gene changes in ALS might also damage motor disorders of the muscles and motor neurons. Your
neurons. doctor inserts electrodes into the muscle, or places
• Environment could also play a role in ALS. Scientists them on the skin overlying a muscle or muscle
are studying whether people who come into contact group to record electrical activity and muscle
with certain chemicals or germs are more likely to get responses.
the disease.
TREATMENT AND MANAGEMENT
Scientists are also looking at these other possible No cure has yet been found for ALS. However, there are
causes: treatments available that can help control symptoms, prevent
unnecessary complications, and make living with the disease
• Glutamate. This chemical sends signals to and from easier.
the brain and nerves. It's a type of neurotransmitter.
With ALS, glutamate builds up in the spaces around MEDICATION
nerve cells and may damage them. • In 1995, the Food and Drug Administration (FDA)
o The medications riluzole (Rilutek) works by approved Riluzole (Rilutek), the only disease-modifying
lowering glutamate levels and can help slow drug to date for ALS.
the development of the disease.. • Although it is not entirely understood how the drug
• Immune system problems. Your immune system works, Riluzole is believed to reduce damage to motor
protects your body from foreign invaders such as neurons by decreasing levels of glutamate, which
bacteria and viruses. In your brain, microglia are the transports messages between nerve cells and motor
main type of immune cell. They destroy germs and neurons.
damaged cells. With ALS, microglia might also • Riluzole does not reverse the damage already done to
destroy healthy motor neurons. motor neurons, and people taking the drug must be
• Mitochondria problems. Mitochondria are the parts monitored for liver damage and other possible side
of your cells where energy is made. A problem with effects. However, this therapy offers hope that the
them might lead to ALS or make an existing case progression of ALS may one day be slowed by new
worse. medications or combinations of drugs.
• Oxidative stress. Your cells use oxygen to make • Physicians can also prescribe medications to help
energy. Some of the oxygen your body uses to make manage symptoms of ALS, including muscle cramps,
energy may form into toxic substances called free stiffness, excess saliva and phlegm, and the
radicals, which can damage cells. The medication pseudobulbar affect (involuntary or uncontrollable
edaravone (Radicava) is an antioxidant that can help episodes of crying and/or laughing, or other emotional
control these free radicals. displays). Drugs also are available to help individuals
with pain, depression, sleep disturbances, and
DIAGNOSIS OF ALS constipation.
There is no specific test to diagnose ALS. A healthcare
provider will consider the medical history and symptoms and PHYSICAL THERAPY
will do certain tests to rule out other conditions including: • Gentle, low-impact aerobic exercise such as walking,
• Lab tests. These include blood and urine studies and swimming, and stationary bicycling can strengthen
thyroid functioning tests. unaffected muscles, improve cardiovascular health, and
• Muscle or nerve biopsy. In this procedure, your help people fight fatigue and depression. Range of
doctor removes a sample of tissue or cells from the motion and stretching exercises can help prevent painful
body and examines it under a microscope. spasticity and shortening (contracture) of muscles.
• Spinal tap (also
called a lumbar SPEECH THERAPY
puncture). In this • As ALS progresses, speech therapists can help people
test, your doctor maintain the ability to communicate. They can
places a special recommend aids such as computer-based speech
needle into the synthesizers that use eye-tracking technology and can
lower back, into help people develop ways for responding to yes-or-no
the area around questions with their eyes or by other nonverbal means.
the spinal cord. Some people with ALS may choose to use voice banking
There he or she while they are still able to speak as a process of storing
can measure the their own voice for future use in computer-based speech
pressure in the synthesizers. These methods and devices help people
spinal canal and communicate when they can no longer speak or produce
brain. Your doctor vocal sounds.
will remove a small
amount of cerebral spinal fluid (CSF) and test it for an
 NUTRITIONAL SUPPORT
• Nutritionists can teach individuals and caregivers how to
plan and prepare small meals throughout the day that
provide enough calories, fiber, and fluid and how to avoid
foods that are difficult to swallow.
• People may begin using suction devices to remove
excess fluids or saliva and prevent choking.
• When individuals can no longer get enough nourishment
from eating, doctors may advise inserting a feeding tube
into the stomach.
• The use of a feeding tube also reduces the risk of
choking and pneumonia that can result from inhaling
liquids into the lungs.

BREATHING SUPPORT
• As the muscles responsible for breathing start to
weaken, people may experience shortness of breath
during physical activity and difficulty breathing at night
or when lying down.
• Doctors may test an individual’s breathing to determine
when to recommend a treatment called noninvasive
ventilation (NIV).

NONINVASIVE VENTILATION (NIV)

– NIV refers to breathing support that is usually delivered
through a mask over the nose and/or mouth. Initially,
NIV may only be necessary at night.
– When muscles are no longer able to maintain normal
oxygen and carbon dioxide levels, NIV may be used
full-time.
– NIV improves the quality of life and prolongs survival for
many people with ALS.
o Because the muscles that control breathing
become weak, individuals with ALS may also
have trouble generating a strong cough
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
TOURETTE’S SYNDROME
GADDAO, CRISTIAN REY I.
MR. ALLAN PAULO BLAQUERA, RN

TOURETTE’S SYNDROME things out" and repeatedly checking to see that

– Tourette syndrome (TS) is a childhood-onset the flame on the stove is turned out.
neuropsychiatric disorder characterized by multiple o Children sometimes repeat a sentence or action
motor and vocal tics that last at least a year in duration many times until it is "just right".
– Typically, the age at onset is between 4 and 6 years, o OCD can include counting rituals, obsessive
peaking in severity around the ages of 10 to 12 years, preoccupations or thoughts which are
with motor tics usually occurring before vocal tics. unpleasant.
– It is a neurological disorder characterized by sudden,
repetitive, rapid, and unwanted movements or vocal • Attention Deficit &/or Hyperactivity Disorder
sounds called tics. (ADD/ADHD) may include difficulty in concentrating,
– Complex vocal tics include the repeated use of words being easily distracted, failing to finish tasks, acting on
or phrases out of context. impulse, not seeming to listen, shifting constantly from
– Coprolalia (use of socially unacceptable words, usually one activity to another, needing a great deal of
obscenities) supervision, being unable to sit still, calling out and lack
– Palilalia (repeating one’s own words) of self-control.
– Echolalia (repeating others’ words) o Adults may have residual signs of ADD such as
overly impulsive behavior and concentration
CAUSES difficulties.
The exact cause of Tourette syndrome isn't known. It's a o Learning Difficulties such as dyslexia, arithmetic
complex disorder likely caused by a combination of inherited and perceptual difficulties, handwriting
(genetic) and environmental factors. Chemicals in the brain problems.
that transmit nerve impulses (neurotransmitters), including
dopamine and serotonin, might play a role. Behavioral problems may include compulsive and repetitive
behaviors, attention problems, sleep difficulties, depression,
SIGNS AND SYMPTOMS poor self-esteem, poor school performance, social isolation,
The motor (involving movements) or vocal (involving sound) school and social phobia. Some commonly observed
tics of Tourette syndrome are classified as either simple or problems include oppositional/defiant behavior, aggressive
complex. They may range from very mild to severe, although and uncooperative behaviors.
most cases are mind.
RISK FOR TOURETTE’S SYNDROME
• Simple Tics – sudden, brief, repetitive movements that • Family history. Having a family history of Tourette
involve a limited number of muscle groups. They are syndrome or other tic disorders might increase the risk
more common than complex tics. of developing Tourette syndrome.
o Motor – eye blinking, head jerking, shoulder • Sex. Males are about three to four times more likely
shrugging, facial grimacing, nose twitching than females to develop Tourette syndrome.
o Vocal – throat clearing, barking noises, • Smoking during pregnancy
squealing, grunting, gulping, sniffing, tongue • Pregnancy complication
clicking • Low birthweight
• Infections
• Complex Tics – distinct, coordinated patterns of
movement involving several muscle groups. THERAPEUTIC MANAGEMENT
o Motor – jumping, touching other people and
things, twirling about, repetitive movements of COMPREHENSIVE BEHAVIORAL INTERVENTION FOR
the torso or limbs, pulling at clothing and self- TICS (CBIT)
injurious actions including hitting or biting
• It is associated with an improvement in symptoms. In
oneself
CBIT, children and teens are taught to recognize the
o Vocal – uttering words or phrase, coprolalia
urge to tic and to use a replacement response instead
(involuntary utterance of inappropriate or
of the tic.
obscene words), echoalia (repeating a sound,
word or phrase just heard) or palilalia (repeating • This includes habit reversal in additional to other
strategies, including education about tics and relaxation
one’s own words)
techniques
People with TS rarely have all of these symptoms. Most • CBIT skills can be learned with practice, with the help of
people will exhibit some or many symptoms over a long an experienced therapist, and with the support and
period of time and in varying degrees: mild, moderate or encouragement of those close to the person with TS
severe. In milder cases a person may have just a few tics or • This incorporates approaches such as habit reversal
twitches, which may be confined to the face, eye and therapy, relaxation training, and learning to identify the
shoulder areas. In more severe cases several areas of the emotions and situations that increase tic severity
body may be affected.
MEDICATIONS
BEHAVIOR PROBLEMS WHICH MAY OCCUR • The alpha2-adrenergic drugs clonidine and
FREQUENTLY IN ADDITION TO TICS guanfacine are first-line agents in treating mild to
moderate tics.
• Obsessive Compulsive Disorder (OCD), in which the o Clonidine decreases plasma norepinephrine
person feels that something must be done over and levels and can also reduce the symptoms of
over. attention deficit–hyperactivity disorder (ADHD).
o Examples include touching an object with one § The daily dosage range for clonidine is
hand after touching it with the other to "even 0.1-0.3 mg in divided doses.
 o Guanfacine, with a similar mechanism of action
as clonidine, has a longer half-life and may treat
ADHD symptoms not responsive to clonidine.
§ For guanfacine, the daily dosage range is
0.5-3.0 mg in divided doses. Clonazepam
and baclofen can be considered first-line
alternatives as well.

• The D2 dopamine receptor—blocking medications

(neuroleptics) are the most effective medications for
treating tics, and many experts use the neuroleptics as
the initial agent of choice for that reason. However, the
side effect profile, which includes extrapyramidal
symptoms/tardive dyskinesia, is often a limitation to
using these agents as first-line therapy.

This syndrome responds to medications that alter the effects

of dopamine, such as haloperidol (Haldol), pimozide
(Orap), or risperidone (Risperdal).

• Haloperidol (Haldol) has been the usual treatment for

Tourette's Syndrome since the 1960's. It is available in
solution form which can be beneficial if a patient
(particularly children) dislikes taking tablets.
o Side effects of Haloperidol:
§ Fatigue
§ Weight gain
§ Memory problems
§ Personality changes
§ Sexual dysfunctions.
o Long term side effects are problematic and can
often be confused with the symptoms of
Tourette's Syndrome. For this reason, some
physicians seek the use of alternative drugs
before Haloperidol.

• Pimozide – (Orap) Although it is called an

antipsychotic, pimozide is more commonly used in the
treatment of movement disorders such as motor and
vocal tics and in patients with Tourette syndrome.
o Pimozide affects the levels of a brain chemical
called dopamine. The exact way pimozide
improves the symptoms of Tourette syndrome
and other conditions is not fully known.
o It has been shown to reduce the number of
motor and vocal tics, as well as the severity of
symptoms. It is generally used after other
treatments for Tourette syndrome such as
haloperidol (Haldol) or risperidone
(Risperdal)are found to be ineffective or
intolerable.

• Risperidone – (Risperdal) a neuroleptic with both

serotonin- and dopamine-blocking properties, appears
to be effective in reducing tic frequency and intensity in
children and adolescents with chronic tic disorders.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
DIABETES MELLITUS (TYPE 1)
DAYAG, CEE JAY MARIE G.
MR. ALLAN PAULO BLAQUERA, RN

period”) generally
TYPE 1 DIABETES MELLITUS after initial
– Type 1 diabetes mellitus is a disorder that involves an diagnosis
absolute or relative deficiency of insulin
– characterized by the destruction of the pancreatic beta A. ASSESSMENT
cells – Although children may be prediabetic for some time, the
– Combined genetic, immunologic, and possibly onset of symptoms in childhood is usually abrupt.
environmental (e.g., viral) factors are thought to – Parents notice increased thirst and increased
contribute to beta-cell destruction urination (which may be recognized first as bed-
– Although the events that lead to beta-cell destruction wetting [enuresis] in a previously toilet-trained child)
are not fully understood, it is generally accepted that a o The dehydration may cause constipation.
genetic susceptibility is a common underlying factor in
the development of type 1 diabetes. LABORATORY STUDIES
– People do not inherit type 1 diabetes itself but rather a – In some children, diabetes is detected at a routine
genetic predisposition, or tendency, toward the health screening
development of type 1 diabetes – For others, although the disease has been progressing
– Diabetic ketoacidosis (DKA) is a metabolic internally for some time, outward symptoms have such
derangement that occurs most commonly in persons an abrupt onset that the child is in a coma from
with type 1 diabetes and results from a deficiency of acidosis and hyperglycemia by the time it is detected.
insulin; highly acidic ketone bodies are formed, and – Laboratory studies usually show a random plasma
metabolic acidosis occurs glucose level greater than 200 mg/dl (normal range, 70
to 110 mg/dl fasting; 90 to 180 mg/dl not fasting) and
The three major metabolic derangements are significant glycosuria
hyperglycemia, ketosis, and metabolic acidosis (Norris,
2019). DKA is commonly preceded by a day or more of ACCEPTABLE BLOOD GLUCOSE RANGES FOR
polyuria, polydipsia, nausea, vomiting, and fatigue with CHILDREN WITH TYPE 1 DM
eventual stupor and coma if not treated. The breath has a
characteristic fruity odor due to the presence of ketoacids. TIMING VALUE (mg/dl)
Before a meal 70 – 110
COMPARISON OF TYPE 1 AND TYPE 2 DM 1 hour after meal 90 – 180
2 hours after meal 80 – 150
ASSESSMENT TYPE 1 TYPE2 Between 2 AM and 4 AM 70 – 120
Age at onset 5-7 or at puberty 40-65 (may occur
in Two diagnostic tests, the fasting blood glucose test and
adolescents as the random blood glucose test, are used to confirm
maturity-onset diabetes. A diagnosis of diabetes is established if one of the
diabetes of youth following three criteria is present on two separate occasions:
[MODY]) • Symptoms of diabetes plus a random blood glucose
Type of onset Abrupt Gradual level greater than 200 mg/dl
Weight changes Marked weight Associated with • A fasting blood glucose level greater than 126 mg/dl
loss often initial obesity • A 2-hour plasma glucose level greater than 200
sign mg/dl during a 75-g oral glucose tolerance test
Other symptoms ü Polydipsia ü Polydipsia (GTT)
ü Polyphagia ü Polyuria
ü Polyuria ü Fatigue ORAL GLUCOSE TOLERANCE TEST
ü Fatigue ü Blurred vision – Typically, it involves the oral ingestion of a concentrated
ü Blurred vision ü Mood changes glucose solution followed by blood glucose levels drawn
ü Mood changes at fasting (baseline), after 1 hour, and after 2 hours.
Therapy • Hypoglycemia • Diet, oral – The test is difficult for children to undergo because
agents never hypoglycemic it requires them to fast for 8 hours, drink an overly
effective; agents, or sweet solution, and submit to painful, intrusive
insulin required insulin procedures (routine application of lidocaine/prilocaine
• No dietary • Nutrition [EMLA] cream to finger stick or venipuncture sites and
foods used; concentrates use of intermittent infusion devices greatly reduces this
should count on no excess problem).
carbohydrates weight gain – REMEMBER: Do not take blood for glucose
plus evaluate and balanced analysis from functioning IV tubing to try to help
blood glucose intake of with pain because the glucose in the IV solution will
levels to help carbohydrates, cause the serum reading to be abnormally high.
determine protein, and fat
insulin dosage. • Meticulous skin
• Commonsense and foot care
foot care for necessary
growing
children
Period of Period of Not
remission remission for 1– demonstrable
12 months
(“honeymoon
OTHER DIAGNOSTIC TOOLS
– If diabetes is detected, the diagnostic workup also COMMON TYPES OF HUMAN INSULIN
usually includes:
Ø analysis of blood samples for Ph PREPARATION ONSET PEAK DURATION
Ø partial pressure of carbon dioxide (PCO2) EFFECT OF
Ø sodium and potassium levels EFFECT
Ø a white blood cell count Lispro Immediate 30mn – 3-4 hr
Ø glycosylated hemoglobin (HbA1c) evaluation. (Humalog) 1hr
Aspart 15 mn 30-40 mn 3-5 hr
If the potassium level of the blood is low, a child may Regular 30mn – 2-4 hr 5-7 hr
need an electrocardiogram to observe for T-wave (Humulin-R) 1hr
abnormalities, the mark of potassium deficiency. The white Lantus 1 hr 5 hr 24 hr
blood cell count of a child with diabetes may be elevated Humulin-N 1-2 hr 4-12 hr 24+ hr
even though no infection is present, apparently as a Humulin-L 1-3 hr 6-14 hr 24+ hr
response to the ketoacidosis. The presence of infection Humulin-U 6 hr 16-18 hr 36+ r
must always be suspected, however, because it is often a
precipitant to a diabetic crisis. For this reason, nose and
A. INSULIN INJECTION
throat cultures may be obtained as well. – Insulin is always injected SC except in
emergencies, when half the required dose may be
B. THERAPEUTIC MANAGEMENT
given IV.
– Therapy for children with type 1 diabetes involves five – Teach parents that when insulins are mixed in one
measures: syringe, the regular or short-acting insulin should
Ø insulin administration be drawn into the syringe first.
Ø regulation of nutrition and exercise – Subcutaneous tissue injection sites used most
Ø stress management
frequently in children include those of the upper
Ø blood glucose and urine ketone monitoring
outer arms and the outer aspects of the thighs
– Encourage children or parents to rotate sites in a
1. INITIAL REGULATION OF INSULIN
pattern based on their planned activity.
– When children are first diagnosed with diabetes,
– Insulin is usually injected at a 90-degree angle
they are usually hyperglycemic and perhaps
with a short needle.
ketoacidotic.
– To correct the metabolic imbalance, they are
Absorption, for example, is increased if the muscles under
given insulin administered IV at a dose of 0.1 to the injection site are exercised, so it is best to choose sites
0.2 units per kilogram of body weight per hour
that will not be exercised soon after the injection. If a child
– This initial IV infusion of insulin is then gradually will be jogging after an injection, for example, the thigh
reduced once the blood glucose level is lower
probably should not be used. Similarly, if the child will be
than 200 mg/dl. playing tennis, the injection probably should not be given in
– Ideally, within 12 hours, the acidosis is the dominant arm
considerably less than when a child was
admitted to the hospital, and the serum glucose B. INSULIN PUMPS
level is near the normal range.
– An insulin pump is an automatic device
– The insulin given for emergency replacement approximately the size of an iPhone. It delivers
this way is regular (short-acting) insulin such as insulin at a constant rate, so it regulates serum
Humulin-R because this is the form that takes glucose levels better than periodic injections
effect most quickly.
– To use a pump, a syringe of regular insulin is
– After 24 hours, as the child’s serum glucose placed in the pump chamber; a length of thin
returns to normal, oral feedings may replace the polyethylene tubing leads to the child’s abdomen,
IV route. where it is implanted into the subcutaneous tissue
– Further management in the days after this first of the abdomen by a small-gauge needle
crucial 24-hour period is based on serum – Most children adjust well to pump therapy and
glucose determinations prefer it to daily injections.
– A child may remain on regular insulin given SC
alone (given three or four times a day) for the C. IHALATION INSULIN
first 1 or 2 days. – Inhalation insulin is not available as yet but may
be in the future; production of it is in experimental
INSULIN ADMINISTRATION trials.
– Children can be regulated on a variety of insulin – Difficulties with development are constructing an
programs, but typically receive a combined insulin dose accurate delivery system and determining how the
of 0.4 to 0.7 units per kilogram of body weight daily in development of a cold or allergies that cause
two divided doses (one before breakfast and one before edema of the nasal membrane will affect drug
dinner); adolescents may need as much as 1.2 units absorption
per kilogram daily divided into the two doses.
– The most common mixture of insulin used with children NUTRITION
is a combination of an intermediate-acting insulin and a – In order to know how much insulin to give before a
regular insulin, usually in a 2:1 ratio or 0.75 units of the meal, parents need to learn to count the total
intermediate-acting insulin to 0.33 units regular insulin, carbohydrate amount in food by carefully reading food
and given in the same syringe, although this labels.
prescription varies for individual children – An insulin-to-carbohydrate ratio is then calculated
individually for each child depending on age and activity
to guide insulin administration
– For example, if a child is prescribed an insulin-to-
carbohydrate ratio of 1 unit of insulin to each 10 g of
 carbohydrates and the meal the child will be served – Try to interview children separately from their parents,
contains 50 g carbohydrates, the parent would so they can feel free to talk about anything that may be
administer 5 units of regular insulin before the meal. happening or going wrong.

An overall meal pattern should include three spaced meals If a child is experiencing stress because of school, parents
that are high in fiber plus a snack in the midmorning, may have to meet with school officials to help them view the
midafternoon, and evening to keep carbohydrate amounts as child as well, not ill, so that they will allow participation in all
level as possible during the day. Most parents need to meet activities, including sports. Sometimes, children are
with a nutritionist to discuss what a “meal high in fiber” embarrassed to have to do blood glucose testing in school,
means, how to become adept at carbohydrate counting, and especially in a public lavatory. It may be easier for them if
what meals are best to serve to their age child. they can go to the nurse’s office for privacy when testing.

SELF-MONITORING OF BLOOD GLUCOSE COMPLICATIONS

– Children as young as early school age can learn the – If an infection occurs and the child’s temperature rises,
techniques of finger puncture and reading a insulin resistance increases, causing a need for
computerized monitor. Using a spring-loaded injection additional insulin. Teach parents to notify their primary
pen helps minimize pain; an automatic readout monitor healthcare provider if their child appears to be ill
simplifies the procedure (particularly if the child is nauseated or vomiting) for
careful observation and a change in insulin dosage if
necessary.
– If a child with diabetes is scheduled for surgery, careful
regulation on the day of surgery and in the immediate
postoperative period is essential, especially if oral fluids
will be restricted.
– Many long-term body changes such as arteriosclerosis
(hardening of artery walls), which can lead to general
poor circulation and kidney disease, and thickening of
retinal capillaries and cataract formation, which
ultimately can result in blindness, occurring because of
chronic hyperglycemia, are not a major part of disease
management in childhood because their onset does not
begin until adulthood.
– It is not too early, however, when discussing
hyperglycemia to mention that it does have long-term
effects if not regulated beginning in childhood.

URINE TESTING PANCREAS TRANSPLANTATION

– Urine testing is not used routinely but is used to test for – For children who develop severe kidney disease or
ketonuria if the child develops a gastrointestinal “flu” arteriosclerosis, pancreas transplantation may be
and is not able to eat. Acetone revealed by a test strip considered to prevent further damage. In contrast to
is a sign fat is being used for energy or that the child is other organ transplantation procedures, the child’s
becoming acidotic pancreas is not removed entirely prior to transplant.
– This is because the portion that supplies digestive
THE “HONEYMOON” PERIOD enzymes is still functioning and so is left in place. The
– After a child’s diagnosis has been confirmed and the digestive enzymes of the new pancreas are diverted
blood glucose level has been initially regulated by into the intestine or bladder, or the pancreatic ducts can
insulin, a honeymoon period may follow, during which be sclerosed, so the digestive enzymes do not leave
only a minimal amount of insulin, or none at all, is the transplanted organ.
needed for glucose regulation – To reduce the child’s immune response and protect
– This apparently occurs because the exogenous insulin against graft rejection, drugs such as antilymphocyte
stimulates the islet cells to produce a small amount of globulin, cyclosporine, prednisone, or azathioprine
natural insulin, as if they are being reminded of their (Imuran) are administered after surgery. If rejection
function. does start to occur, the patient is given monoclonal T-
cell antibodies (OKT3) to try to reverse this process.
After a month or even up to a year, however, the islet cells
will begin to fail once again, and diabetic symptoms will Pancreatic transplantation is a last resort solution for children
recur. This can be upsetting to parents if they began to because it involves major surgery, the outcome is guarded
believe their child was wrongly diagnosed or that a cure had (about 50% of transplanted organs are rejected), and the
taken place. Caution both the parents and the child that result—continuous immunosuppressive medication for life—
symptoms will inevitably recur may not be regarded as a major improvement over the
original illness, which requires continuous daily insulin for
STRESS ADJUSTMENT life. In addition, some pancreatic transplant recipients have a
– Whenever children with diabetes undergo a stressful recurrence of diabetes
situation, either emotionally or physically, they may
need increased insulin to maintain glucose
homeostasis.
– When children are seen at healthcare facilities for
periodic checkups, ask them whether they are having
any difficulty with blood testing or insulin injection and
how things are at home and at school to detect their
stress level.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
FLUID AND ELECTROLYTE IMBALANCE
DAYAG, CEE JAY MARIE G.
MR. ALLAN PAULO BLAQUERA, RN

FLUID AND ELECTROLYTE IMBALANCES – This might occur in a child with nausea (thus preventing
– Because the GI system is the main route by which fluid intake) and fever (which increases fluid loss
substances are taken into the body, it can be a major through perspiration); profuse diarrhea, where there is a
source of fluid and electrolyte loss if vomiting or greater loss of fluid than salt; or renal disease
diarrhea occurs associated with polyuria such as nephrosis with
– Retaining fluid is of greater importance in the body diuresis.
chemistry of infants than that of adults because fluid – Electrolytes such as sodium, chloride, and bicarbonate
constitutes a greater fraction of the infant’s total weight. concentrate in the blood.
In adults, body water accounts for approximately 60% – The red blood cell count and hematocrit will be elevated
of total weight. because the blood is more concentrated than usual.

Fluid is distributed in three body compartments: (a) E. HYPOTONIC DEHYDRATION

intracellular (within cells), 35% to 40% of body weight; (b) – With hypotonic dehydration, there is a
interstitial (surrounding cells), 20% of body weight; and (c) disproportionately high loss of electrolytes in proportion
intravascular (blood plasma), 5% of body weight. Together, to fluid loss.
the interstitial and the intravascular fluid are often referred to – The plasma concentration of sodium and chloride are
as extracellular fluid (ECF), totaling 25% of body weight. In low. This could result from excessive loss of
infants, the ECF portion is much greater, totaling up to 45% electrolytes by vomiting, from an increased loss of salt
of total body weight from diuresis, or from diseases such as adrenocortical
insufficiency or diabetic acidosis.
– Fluid is normally obtained by the body through oral – In order to achieve an electrolyte balance, the kidneys
ingestion of fluid and by the water formed in the begin to excrete more fluid to bring the proportion of
metabolic breakdown of food. Primarily, fluid is lost from electrolytes and fluid back in balance, leading to a
the body in urine and feces secondary extracellular dehydration
– Minor losses (insensible losses) occur from evaporation
from skin and lungs and from saliva, which is of little SIGNS AND SYMPTOMS OF DEHYDRATION
importance except in children with tracheostomies or
those requiring nasopharyngeal suction. ISOTONIC HYPOTONIC HYPERTONIC
– When diarrhea occurs, or when a child becomes Thirst Mild Moderate Extreme
diaphoretic because of fever, the fluid output can be Skin Poor Very poor Moderate
markedly increased, quickly leading to dehydration turgor
(excessive loss of fluid) Skin Dry Clammy Moderate
consistenc
MAIN ELECTROLYTES IN THE BODY y
Skin temp Cool Cool Warm
Urine Decreased Decreased Decreased
output
Activity Irritable Lethargic Very lethargic
Serum Normal Reduced Increased
sodium
level

F. OVERHYDRATION
– or excessive body fluid intake, can be as serious as
dehydration. It generally occurs in children who are
receiving IV fluid and can lead to cardiovascular and
cardiac failure.
– When large quantities of salt-poor fluid (hypotonic
solutions) such as tap water are ingested or are given
by enema, the body transfers water from the
FLUID VOLUME IMBALANCES extracellular space into the intracellular space to restore
– Under most circumstances, water and salt are lost in normal osmotic relationships
proportion to each other, termed isotonic dehydration. – This transfer results in intracellular edema manifested
– Occasionally, water is lost out of proportion to salt, and by a headache, nausea, vomiting, dimness and blurring
water depletion or hypertonic dehydration occurs. of vision, cramps, muscle twitching, and seizures.
– If electrolytes are lost out of proportion to water, this is – A situation in which intracellular edema may occur is
termed hypotonic dehydration. Each of these abnormal when tap water enemas are given to a child with
states produces specific symptoms. aganglionic disease of the intestines

C. ISOTONIC DEHYDRATION
– occurs when a child’s body loses more water than it
absorbs (as with diarrhea) or absorbs less fluid than it
excretes (as with nausea and vomiting).
– The main result of isotonic dehydration is a decrease in
the volume of blood serum.

D. HYPERTONIC DEHYDRATION
– When water is lost in a greater proportion than
electrolytes, hypertonic dehydration occurs.
 I. FLUID VOLUME DISTURBANCES Ø decreased intake, as in nausea or lack of
access to fluids
IMBALANCE CONTRIBUTING SIGNS/SYMPTOMS Ø and third-space fluid shifts, or the
FACTORS AND LAB FINDINGS movement of fluid from the vascular
Hypovolemia Loss of water and Acute weight loss, ↓ system to other body spaces (e.g., with
electrolytes, as in skin turgor, oliguria, edema formation in burns, ascites with
vomiting, diarrhea, concentrated urine, liver dysfunction).
fistulas, fever, capillary filling time – Additional causes include:
excess sweating, prolonged, low CVP, ↓ Ø diabetes insipidus (a decreased ability to
burns, blood loss, BP, flattened neck concentrate urine due to either a deficit of
gastrointestinal veins, dizziness, ADH or nephron resistance to ADH)
suction, and weakness, thirst and Ø adrenal insufficiency
thirdspace fluid confusion, ↑ pulse, Ø osmotic diuresis
shifts; and muscle cramps, Ø hemorrhage
decreased intake, sunken eyes, nausea, Ø coma
as in anorexia, increased
nausea, and temperature; cool, B. ASSESSMENT AND DIAGNOSTIC FINDINGS
inability to gain clammy, pale skin – Laboratory data used to evaluate fluid volume status
access to fluid. include BUN and its relation to serum creatinine
Diabetes insipidus Labs indicate: ↑ concentration.
and uncontrolled hemoglobin and – The presence and cause of hypovolemia may be
diabetes both hematocrit, ↑ serum determined through the health history and physical
contribute to a and urine osmolality examination.
depletion of and specific gravity, ↓ o In addition, the hematocrit level is greater than
extracellular fluid urine sodium, ↑ BUN normal because there is a decreased plasma
volume. and creatinine, ↑ urine volume, which concentrates the volume of
specific gravity and RBCs.
osmolality – Serum electrolyte changes may also exist. Potassium
Hypervolemia Compromised Acute weight gain, and sodium levels can be reduced (hypokalemia,
regulatory peripheral edema and hyponatremia) or elevated (hyperkalemia,
mechanisms, such ascites, distended hypernatremia).
as kidney injury, jugular veins, o Hypokalemia can occur with GI and renal
heart failure, and crackles, elevated losses as these organs are major regulators of
cirrhosis; CVP, shortness of potassium.
overzealous breath, ↑ BP, o Hyperkalemia can occur with adrenal
administration of bounding pulse and insufficiency due to aldosterone deficiency
sodium-containing cough, ↑ respiratory which causes lack of potassium excretion.
fluids; and fluid rate, ↑ urine output o Hyponatremia can occur with increased thirst
shifts (i.e., and ADH release, which increases water
treatment of burns). Labs indicate: ↓ content of the bloodstream.
Prolonged hemoglobin and o Hypernatremia can result from increased
corticosteroid hematocrit, ↓ serum insensible water losses and diabetes insipidus
therapy, severe and urine osmolality, ↓
stress, and urine sodium and Oliguria, the excretion of less than 400 mL urine per day in
hyperaldosteronism specific gravity the adult, may or may not be present in hypovolemia. Urine
augment fluid specific gravity will change in relation to the kidneys’ attempt
volume excess. to conserve water. If the kidney does not reabsorb water,
urine contains more water, and urine specific gravity is low. If
HYPOVOLEMIA the kidney does reabsorb water, urine will be concentrated
– FVD, or hypovolemia, occurs when loss of ECF volume and specific gravity increases.
exceeds the intake of fluid. It occurs when water and
C. MEDICAL MANAGEMENT
electrolytes are lost in the same proportion as they exist
in normal body fluids; thus, the ratio of serum electrolytes – primary provider considers the patient’s maintenance
requirements and other factors (e.g., fever) that can
to water remains the same.
influence fluid needs
– FVD may occur alone or in combination with other
imbalances. Serum electrolyte concentrations can remain – If the deficit is not severe, the oral route is preferred,
normal, increase, or increase in FVD provided the patient can drink. However, if fluid losses
are acute or severe, the IV route is required.
FVD should not be confused with dehydration, which refers – Isotonic electrolyte crystalloid solutions (e.g., lactated
to loss of water alone, with increased serum sodium levels. Ringer’s solution or 0.9% sodium chloride) are
frequently the first-line choice to treat the hypotensive
A. PATHOPHYSIOLOGY patient with FVD because they expand plasma volume.
– FVD results from loss of body fluids and occurs more – Accurate and frequent assessments of I&O, weight,
rapidly when coupled with decreased fluid intake vital signs, central venous pressure, level of
consciousness, breath sounds, and skin color are
– FVD results from loss of body fluids and occurs more
rapidly when coupled with decreased fluid intake monitored to determine when therapy should be slowed
to avoid volume overload.
– Causes of FVD include abnormal fluid losses, such as
those resulting from: – If the patient with severe FVD is not excreting enough
Ø Vomiting urine and is therefore oliguric, the primary provider
needs to determine whether the depressed renal
Ø Diarrhea
Ø GI suctioning function is caused by reduced renal blood flow
secondary to FVD (prerenal azotemia) or, more
Ø Sweating
 seriously, by acute tubular necrosis (intrarenal substances, the serum sodium concentration remains
azotemia) from prolonged FVD essentially normal.

D. NURSING MANAGEMENT A. PATHOPHYSIOLOGY

– To assess for FVD, the nurse monitors and measures – FVE may be related to simple fluid overload or
fluid I&O at least every 8 hours, and sometimes hourly diminished function of the homeostatic mechanisms
o Maintaining an accurate I&O is a particular responsible for regulating fluid balance
challenge with patients in critical-care settings. – Contributing factors can include heart failure, kidney
– As FVD develops, body fluid losses exceed fluid intake dysfunction, and cirrhosis of the liver.
through excessive urination (polyuria), diarrhea, – Another contributing factor is consumption of excessive
vomiting, or other mechanisms Once FVD has amounts of table or other sodium salts. Excessive
developed, the kidneys attempt to conserve body fluids, administration of sodium-containing fluids in a patient
leading to a urine output of less than 1 mL/kg/h in an with impaired regulatory mechanisms may predispose
adult. Urine in this instance is concentrated and them to a serious FVE as well
represents a healthy renal response.
– Vital signs should be closely monitored in FVD. B. CLINICAL MANIFESTATIONS
o A decrease in body temperature often – Clinical manifestations of FVE result from expansion of
accompanies FVD, unless there is a concurrent the ECF and may include
infection Ø edema
– Skin and tongue turgor are monitored on a regular Ø distended jugular veins
basis. In a healthy person, pinched skin immediately Ø crackles (abnormal lung sounds due to
returns to its normal position when released interstitial pulmonary fluid).
– Urine concentration is monitored by measuring the – In patients who are ambulatory, edema is most evident
urine specific gravity. In a volume-depleted patient, the in the ankles; in patients who are supine, edema occurs
urine specific gravity should be greater than 1.020, over the sacrum
indicating healthy renal conservation of fluid. Dark
amber-colored urine is highly concentrated; whereas, C. ASSESSMENT AND DIAGNOSTIC FINDINGS
clear yellow urine indicates a dilute urine. – Laboratory data useful in diagnosing FVE include BUN
– Mental function is eventually affected, resulting in and hematocrit levels. In FVE, both of these values may
confusion, lack of cognition, and delirium in severe FVD be decreased because of plasma dilution
as a result of decreasing cerebral perfusion. Behavioral – In chronic kidney disease, both serum osmolality and
changes are particularly evident in older adults with the sodium level are decreased due to excessive
FVD. Decreased peripheral perfusion can result in cold retention of water. The urine sodium level is increased if
extremities the kidneys are attempting to excrete excess volume.
– A chest x-ray may reveal pulmonary congestion in FVE
PREVENTING HYPOVOLEMIA – Hypervolemia occurs when aldosterone is chronically
– To prevent FVD, the nurse identifies patients at risk and stimulated—for example, in conditions such as
takes measures to minimize fluid losses cirrhosis, heart failure, and nephrotic syndrome.
o If the patient has diarrhea, measures should be – Aldosterone increases both sodium and water
implemented to control diarrhea and reabsorption into the bloodstream from the nephron;
replacement fluids given. This includes therefore, the urine sodium level is normal in these
administering antidiarrheal medications and conditions
small volumes of oral fluids at frequent intervals.
D. PHARMACOLOGIC THERAPY
CORRECTING HYPOVOLEMIA – Diuretics are prescribed when dietary restriction of
– When possible, oral fluids are given to help correct sodium alone is insufficient to reduce edema.
FVD, with consideration given to the patient’s likes and – The choice of diuretic is based on the severity of the
dislikes hypervolemic state, the degree of impairment of renal
– The type of fluid the patient has lost is also considered, function, and the potency of the diuretic.
and fluids most likely to replace the lost electrolytes are – Thiazide diuretics block sodium and water reabsorption
appropriate. into the bloodstream at the distal tubule of the nephron,
– If the patient is reluctant to drink because of oral where 5% to 10% of sodium is normally reabsorbed.
discomfort, the nurse assists with frequent mouth care o This leads to a small amount of sodium and
and provides nonirritating fluids. water loss via the urine.
– The patient may be offered small volumes of oral – Loop diuretics, such as furosemide, bumetanide, or
rehydration solutions torsemide, can cause a greater loss of both sodium and
– These solutions provide fluid, glucose, and electrolytes water because they block sodium reabsorption in the
in concentrations that are easily absorbed. ascending limb of the loop of Henle, where 20% to 30%
– If nausea is present, an antiemetic may be needed of filtered sodium is normally reabsorbed
before oral fluid replacement can be tolerated
Generally, thiazide diuretics, such as hydrochlorothiazide,
HYPERVOLEMIA are prescribed for mild to moderate hypervolemia and loop
– Fluid volume excess (FVE), or hypervolemia, refers to diuretics for severe hypervolemia (Brater & Ellison, 2019).
an expansion of the ECF caused by the abnormal
retention of water and sodium in approximately the E. NURSING MANAGEMENT
same proportions in which they normally exist in the – To assess for FVE, the nurse measures I&O at regular
ECF intervals to identify excessive fluid retention
– It is most often secondary to an increase in the total- – The patient is weighed daily, and rapid weight gain is
body sodium content, which, in turn, leads to an noted.
increase in total-body water. – Breath sounds are assessed at regular intervals in at-
– This can be referred to as an isotonic accumulation of risk patients, particularly if parenteral fluids are being
fluids. Because there is isotonic retention of body given
 – The nurse monitors the degree of edema in the most water irritability, simple
dependent parts of the body, such as the feet and supplements, partial or tonic–clonic
ankles in ambulatory patients and the sacral region in diabetes insipidus, seizures, pulmonary
patients confined to bed. heatstroke, edema, hyperreflexia,
– Pitting edema is assessed by pressing a finger into the hyperventilation, twitching, nausea,
affected part, creating a pit or indentation that is watery diarrhea, vomiting, anorexia, ↑
evaluated on a scale of 1+ (minimal) to 4+ (severe) burns, and pulse, and ↑ BP
– Peripheral edema is monitored by measuring the diaphoresis.
circumference of the extremity with a tape measure Excess Labs indicate: ↑
marked in millimeters corticosteroid, serum sodium, ↓ urine
sodium sodium, ↑ urine
PREVENTING HYPERVOLEMIA bicarbonate, and specific gravity and
– Specific interventions vary with the underlying condition sodium chloride osmolality, ↓ CVP
and the degree of FVE. However, most patients require administration,
sodium-restricted diets in some form, and adherence to and saltwater
the prescribed diet is encouraged. nonfatal drowning
– Patients are instructed to avoid over-the-counter (OTC) victims.
medications without first checking with a health care
provider, because they may contain sodium SODIUM DEFICIT (HYPONATREMIA)
– If fluid retention persists despite adherence to a – refers to a serum sodium level that is less than 135
prescribed diet, hidden sources of sodium, such as the mEq/L (135 mmol/L)
water supply or use of water softeners, should be – can present as an acute or chronic form
considered. o Acute hyponatremia is commonly the result of a
fluid overload in a surgical patient. This is a
II. ELECTROLYTLE IMBALANCES dilutional hyponatremia because the excess
– Disturbances in electrolyte balances are common in water dilutes the sodium in the bloodstream.
clinical practice and may need to be corrected based on o Chronic hyponatremia is seen more frequently in
history, physical examination findings, and laboratory patients outside the hospital setting, has a
values (with comparison to previous values). longer duration, and has less serious neurologic
sequelae.
SODIUM IMBALANCES o Another type of hyponatremia is exercised-
associated hyponatremia, which is more
IMBALANCE CONTRIBUTING SIGNS/SYMPTOMS frequently found in women and those of smaller
FACTORS AND LAB FINDINGS stature. It can occur during extreme
Sodium deficit Loss of sodium, Anorexia, nausea and temperatures, because of excessive fluid intake
(hyponatremia) as in use of vomiting, headache, before exercise, or prolonged exercise that
Serum sodium diuretics, loss of lethargy, dizziness, results in excess loss of sodium through
<135 mEq/L GI fluids, renal confusion, muscle perspiration
disease, and cramps and
adrenal weakness, muscular A. PATHOPHYSIOLOGY
insufficiency. Gain twitching, seizures, – primarily occurs due to an imbalance of water rather
of water, as in papilledema, dry skin, than sodium
excessive ↑ pulse, ↓ BP, weight o Checking the urine sodium value can assist in
administration of gain, edema differentiating renal from nonrenal causes of
D5W and water hyponatremia.
supplements for Labs indicate: ↓ – Low sodium in the urine occurs as the nephrons of the
patients receiving serum and urine kidney retain sodium to compensate for nonrenal fluid
hypotonic tube sodium, ↓ urine loss (i.e., vomiting, diarrhea, sweating). High sodium
feedings; disease specific gravity and concentration in the urine is associated with renal salt
states associated osmolality wasting that occurs in renal dysfunction or diuretic use.
with SIADH, such In dilutional hyponatremia, the ECF volume has excess
as head trauma water but there is no edema, and the excess water
and oat-cell lung dilutes the sodium
tumor;
medications B. CLINICAL MANIFESTATIONS
associated with – Clinical manifestations of hyponatremia depend on the
water retention cause, magnitude, and speed with which the deficit
(oxytocin and occurs.
certain – Poor skin turgor, dry mucosa, headache, decreased
tranquilizers); and saliva production, orthostatic fall in blood pressure,
psychogenic nausea, vomiting, and abdominal cramping can occur.
polydipsia. – Neurologic changes, including altered mental status,
Hyperglycemia status epilepticus, and coma, are related to the cellular
and heart failure swelling and cerebral edema associated with
cause a loss of hyponatremia.
sodium. – As the extracellular sodium level decreases, the cellular
Sodium excess Fluid deprivation Thirst, elevated body fluid becomes relatively more concentrated and pulls
(hypernatremia) in patients who temperature, swollen water into the cells
Serum sodium cannot respond to dry tongue and sticky – In general, patients with an acute decrease in serum
>145 mEq/L thirst, hypertonic mucous membranes, sodium levels have more cerebral edema and higher
tube feedings hallucinations, mortality rates than do those with more slowly
without adequate lethargy, restlessness, developing hyponatremia
– Acute decreases in sodium, developing in less than 48 – The nurse needs to get a thorough history to identify if
hours, may be associated with cerebral edema. the patient is a performance athlete. Performance
– Cerebral edema can lead to compression of brain stem athletes (i.e., marathon runners) may use salt tablets to
structures and brain herniation. compensate for loss of sodium with sweating, hoping to
– Chronic decreases in sodium, developing over 48 hours decrease sodium loss during prolonged exercise;
or more, can occur in status epilepticus and other however, there is no evidence that this practice works
neurologic conditions and it is not recommended
– Hyponatremia is a frequently overlooked cause of
Clinical features of hyponatremia associated with sodium confusion in older patients, who are at increased risk
loss and water gain include anorexia, muscle cramps, and because of decreased renal function and subsequent
a feeling of exhaustion. The severity of symptoms inability to excrete excess fluids
increases with the degree of hyponatremia and the speed
with which it develops. When the serum sodium level SODIUM EXCESS (HYPERNATREMIA)
decreases to less than 115 mEq/L (115 mmol/L), signs of – Hypernatremia is a serum sodium level higher than 145
increasing intracranial pressure, such as lethargy, mEq/L (145 mmol/L). It can be caused by a gain of
confusion, muscle twitching, focal weakness, sodium in excess of water or by a loss of water in
hemiparesis, papilledema, seizures, and death, may excess of sodium.
occur – It can occur in patients with normal fluid volume or in
those with FVD or FVE.
B. ASSESSMENT AND DIAGNOSTIC FINDINGS – With water loss, the patient loses more water than
– Targeted assessment includes the history and physical sodium; as a result, the serum sodium concentration
examination with a focused neurologic examination; increases and the increased concentration pulls fluid
evaluation of signs and symptoms as well as laboratory out of the cell.
test results; identification of current IV fluids, if – This is both an extracellular and an intracellular FVD. In
applicable; and a review of all medications the patient is sodium excess, the patient ingests or retains more
taking sodium than water
– Regardless of the cause of hyponatremia, the serum
sodium level is less than 135 mEq/L; in SIADH, it may A. PATHOPHYSIOLOGY
be lower than 100 mEq/L (100 mmol/L). – A common cause of hypernatremia is fluid deprivation
– Serum osmolality is usually decreased. When in patients who do not respond to thirst
hyponatremia is due to lack of sodium ingestion, the – Most often affected are patients who are very old, very
urinary sodium content is less than 20 mEq/L (20 young, or cognitively impaired.
mmol/L) and the specific gravity is low (1.002 to 1.004). – Administration of hypertonic enteral feedings without
adequate water supplements leads to hypernatremia,
C. SODIUM REPLACEMENT as does watery diarrhea and greatly increased
– The most common treatment for hyponatremia is insensible water loss through the lungs or skin (e.g.,
careful administration of sodium by mouth, nasogastric hyperventilation, burns)
tube, or a parenteral route. – In addition, diabetes insipidus, which is a lack of ADH
– For patients who can eat and drink, sodium is easily due to posterior pituitary dysfunction, can lead to lack of
replaced, because sodium is consumed abundantly in a adequate reabsorption of water into the bloodstream at
normal diet. the level of the nephron.
– For those who cannot consume sodium, lactated – This leads to inadequate water volume in the
Ringer’s solution or isotonic saline (0.9% sodium bloodstream which leads to hypernatremia if the patient
chloride) solution may be prescribed. does not respond to thirst, or if fluids are excessively
– Serum sodium must not be increased by more than 12 restricted
mEq/L in 24 hours to avoid neurologic damage due to – Less common causes of hypernatremia are heatstroke,
demyelination nonfatal drowning in seawater (which contains a
sodium concentration of approximately 500 mEq/L),
D. WATER RESTRICTION and malfunction of hemodialysis or peritoneal dialysis
– In patients with normal or excess fluid volume, systems.
hyponatremia is usually treated effectively by restricting – IV administration of hypertonic saline or excessive use
fluid. of sodium bicarbonate also causes hypernatremia
o However, if neurologic symptoms are severe
(e.g., seizures, delirium, coma), or in patients B. CLINICAL MANIFESTATION
with traumatic brain injury, it may be necessary – The clinical manifestations of hypernatremia are due to
to administer small volumes of a hypertonic increased plasma osmolality caused by an increase in
sodium solution with the goal of alleviating plasma sodium concentration
cerebral edema. o Water moves out of the cell into the ECF,
resulting in cellular dehydration
Incorrect use of these fluids is extremely dangerous, – Dehydration (resulting in hypernatremia) is often
because 1 L of 3% sodium chloride solution contains 513 overlooked as the cause of mental status and
mEq of sodium and 1 L of 5% sodium chloride solution behavioral changes in older patients
contains 855 mEq of sodium. The recommendation for – Body temperature may increase mildly, but it returns to
hypertonic saline administration in patients with normal after the hypernatremia is corrected.
craniocerebral trauma is 3% saline between 0.10 and 1.0
mL/kg of body weight per hour A primary characteristic of hypernatremia is thirst. Thirst is a
strong defender of normal serum sodium levels in healthy
E. NURSING MANAGEMENT people. Because of thirst, hypernatremia does not occur
– The nurse needs to identify and monitor patients at risk unless the person is unconscious or cannot access water.
for hyponatremia. The nurse monitors I&O as well as However, those who are ill and older adults may have an
daily body weight. I&O can be used to identify excess impaired thirst mechanism
water input or lack of sufficient water output
 C. ASSESSMENT AND DIAGNOSTIC FINDINGS sodium– potassium pump, potassium is constantly being
– the serum sodium level exceeds 145 mEq/L (145 pumped into the cells.
mmol/L) and the serum osmolality exceeds 300
mOsm/kg (300 mmol/L).
– The urine specific gravity and urine osmolality are
increased as the kidneys attempt to conserve water
(provided the water loss is from a route other than the IMBALANCE CONTRIBUTING SIGNS/SYMPTOMS
kidneys). FACTORS AND LAB
– Patients with diabetes insipidus do not reabsorb water FINDINGS
into the bloodstream at the nephron Potassium Diarrhea, vomiting, Fatigue, anorexia,
o These patients consequently develop excess deficit gastric suction, nausea and
urine output, dehydration, and hypernatremia (hypokalemia) corticosteroid vomiting, muscle
– Without ADH, these patients excrete very dilute urine Serum administration, weakness, polyuria,
with a urine osmolality less than 250 mOsm/kg potassium hyperaldosteronism, decreased bowel
<3.5 mEq/L carbenicillin, motility, ventricular
D. NURSING MANAGEMENT amphotericin B, asystole or
– Fluid losses and gains are carefully monitored in bulimia, osmotic fibrillation,
patients who are at risk for hypernatremia diuresis, alkalosis, paresthesias, leg
– The nurse should assess for abnormal losses of starvation, diuretics, cramps, ↓ BP, ileus,
water or low water intake and for large gains of and digoxin toxicity abdominal
sodium, as might occur with ingestion of OTC distention,
medications that have a high sodium content hypoactive reflexes.
o the nurse obtains a medication history,
because some prescription medications have ECG: flattened T
a high sodium content. waves, prominent U
– The nurse also notes the patient’s thirst or elevated waves, ST
body temperature and evaluates it in relation to other depression,
clinical signs and symptoms. prolonged PR
– The patient is monitored closely for changes in interval
behavior, such as restlessness, disorientation, and Potassium Pseudohyperkalemia, Muscle weakness,
lethargy excess oliguric kidney injury, tachycardia →
(hyperkalemia) use of potassium- bradycardia,
PREVENTING HYPERNATREMIA Serum conserving diuretics arrhythmias, flaccid
– The nurse attempts to prevent hypernatremia by potassium in patients with renal paralysis,
providing oral fluids at regular intervals, particularly in >5.0 mEq/L insufficiency, paresthesias,
patients who are unable to perceive or respond to metabolic acidosis, intestinal colic,
thirst. Addison disease, cramps, abdominal
– If fluid intake remains inadequate or the patient is crush injury, burns, distention, irritability,
unconscious, the nurse consults with the primary stored bank blood anxiety.
provider to plan an alternative route for intake, either transfusions, rapid IV
by enteral feedings or by the parenteral route. administration of ECG: tall tented T
– If enteral feedings are used, sufficient water should potassium, and waves, prolonged
be given to keep the serum sodium and BUN within certain medications PR interval and
normal limits. such as ACE QRS duration,
– As a rule, the higher the osmolality of the enteral inhibitors, NSAIDs, absent P waves, ST
feeding, the greater is the need for water cyclosporine depression
supplementation
– For patients with diabetes insipidus, adequate water
intake must be ensured. If the patient is alert and has POTASSIUM DEFICIT (HYPOKALEMIA)
an intact thirst mechanism, merely providing access – Hypokalemia (serum potassium level below 3.5 mEq/L
to water may be sufficient. [3.5 mmol/L]) usually indicates a deficit in total
– If the patient has a decreased level of consciousness potassium stores
or other disability interfering with adequate fluid o However, it may occur in patients 794 with
intake, parenteral fluid replacement may be normal potassium stores
prescribed. – When alkalosis (high blood pH) is present, a temporary
shift of serum potassium into the cells occurs
POTASSIUM IMBALANCES
– Potassium (K+) is the major intracellular electrolyte; in A. PATHOPHYSIOLOGY
fact, 98% of the body’s potassium is inside the cells. – Potassium-losing diuretics, such as the thiazides and
– The remaining 2% is in the ECF and is important to loop diuretics, can induce hypokalemia.
neuromuscular and cardiac function. – Other medications that can lead to hypokalemia include
– Potassium influences both skeletal and cardiac corticosteroids, sodium penicillin, and amphotericin B
muscle activity. – GI loss of potassium is another common cause of
– Potassium imbalances are commonly associated with potassium depletion.
various diseases, injuries, medications (e.g., NSAIDs – Vomiting and gastric suction frequently lead to
and ACE inhibitors), and acid–base imbalances hypokalemia, because potassium is lost when gastric
– The normal serum potassium concentration ranges fluid is lost and because potassium is lost through the
from 3.5 to 5 mEq/L (3.5 to 5 mmol/L), and even kidneys in response to metabolic alkalosis
minor variations are significant o Because relatively large amounts of potassium
are contained in intestinal fluids, potassium
For example, alterations in K+ concentration can change deficit occurs frequently with diarrhea, which
myocardial irritability and rhythm. Under the influence of the may contain as much potassium as 30 mEq/L.
– Potassium deficit also occurs from prolonged intestinal For example, patients receiving digitalis who are at risk for
suctioning, recent ileostomy, and villous adenoma (a potassium deficiency should be monitored closely for signs
tumor of the intestinal tract characterized by excretion of digitalis toxicity, because hypokalemia potentiates the
of potassium-rich mucus) action of digitalis.
– Insulin promotes the entry of potassium into cells from
the bloodstream; therefore, patients with persistent PREVENTING HYPOKALEMIA
insulin hypersecretion may experience hypokalemia. – The nurse helps prevent hypokalemia by encouraging
Patients receiving high carbohydrate parenteral patients at risk to eat foods rich in potassium (when the
nutrition will have increased secretion of insulin. This diet allows).
will cause the shift of potassium into the cells from the – Consumption of foods high in potassium should be
bloodstream, causing hypokalemia. encouraged; examples include bananas, melon, citrus
– In diabetic ketoacidosis (DKA), potassium moves out of fruits, fresh and frozen vegetables (avoid canned
the cell since H+ ions are high; during this acute phase vegetables), lean meats, milk, and whole grains
it seems as though the patient has hyperkalemia. With – If the hypokalemia is caused by abuse of laxatives or
insulin 795 treatment of DKA, potassium moves back diuretics, patient education may help alleviate the
into the cells, causing hypokalemia problem.
– Patients who are not able to eat a normal diet for a o Part of the health history and assessment
prolonged period are at risk for hypokalemia. This may should be directed at identifying problems that
occur in debilitated older adults and in patients with are amenable to prevention through education
alcoholism or anorexia nervosa. – Careful monitoring of fluid I&O is necessary, because
o In addition to poor intake, people with bulimia 40 mEq of potassium is lost for every liter of urine
frequently experience increased potassium loss output. The ECG is monitored for changes, and arterial
through self-induced vomiting and overuse of blood gas (ABG) values are checked for elevated
laxatives, diuretics, and enemas. bicarbonate and pH levels.
o These patients may also be deficient in
magnesium. Magnesium depletion also causes ADMINISTERING INTRAVENOUS POTASSIUM
renal potassium loss and must be corrected first; – Potassium should be given only after adequate urine
otherwise, urine loss of potassium will continue output has been established.
– A decrease in urine volume to less than 20 mL/h for 2
B. CLINICAL MANIFESTATION consecutive hours is an indication to stop the potassium
– Potassium deficiency can result in widespread infusion and notify the primary provider
derangements in physiologic function. – Potassium is primarily excreted by the kidneys; when
– Severe hypokalemia can cause death through cardiac oliguria occurs, potassium administration can cause the
or respiratory arrest. serum potassium concentration to rise to dangerous
– Clinical signs develop when the potassium level levels
decreases to less than 3 mEq/L (3 mmol/L) – Administration of IV potassium is done with extreme
– If prolonged, hypokalemia can lead to an inability of the caution using an infusion pump with the patient
kidneys to concentrate urine, causing dilute urine monitored by continuous ECG
(resulting in polyuria, nocturia) and excessive thirst. – Renal function should be monitored through BUN and
– Potassium depletion suppresses the release of insulin serum creatinine levels and urine output if the patient is
and results in glucose intolerance receiving potassium replacement.
– During replacement therapy, the patient should be
C. ASSESSMENT AND DIAGNOSTIC FINDINGS monitored for signs of worsening hypokalemia as well
– In hypokalemia, the serum potassium concentration is as hyperkalemia.
less than the lower limit of normal, which is 3.5 mEq/L.
Electrocardiographic (ECG) changes can include flat T POTASSIUM EXCESS (HYPERKALEMIA)
waves or inverted T waves or both, suggesting – Hyperkalemia (serum potassium level greater than 5
ischemia, and depressed ST segments mEq/L [5 mmol/L]) seldom occurs in patients with
o An elevated U wave is specific to hypokalemia. normal renal function
– Metabolic alkalosis is commonly associated with – In older adults, there is an increased risk of
hypokalemia. This is discussed further in the section on hyperkalemia due to decreases in renin and
acid–base disturbances in this chapter. aldosterone as well as an increased number of
– The source of the potassium loss is usually evident comorbid cardiac conditions
from a careful history. However, if the cause of the loss – Like hypokalemia, hyperkalemia is often caused by
is unclear, a 24-hour urinary potassium excretion test iatrogenic (treatment-induced) causes.
can be performed to distinguish between renal and – Although hyperkalemia is less common than
extrarenal loss hypokalemia, it is usually more dangerous because
– Urinary potassium excretion exceeding 20 mEq/day cardiac arrest is more frequently associated with high
with hypokalemia suggests that renal potassium loss is serum potassium levels
the cause.
A. PATHOPHYSIOLOGY
D. NURSING MANAGEMENT – Major causes of hyperkalemia are decreased renal
– Because hypokalemia can be life-threatening, the nurse excretion of potassium, rapid administration of
needs to monitor for its early presence in patients at potassium, and movement of potassium from the ICF
risk. compartment to the ECF compartment.
– Fatigue, anorexia, muscle weakness, decreased bowel – Hyperkalemia is commonly seen in patients with
motility, paresthesias, and arrhythmias are signals that untreated kidney injury, particularly those in whom
warrant assessing the serum potassium concentration potassium levels increase as a result of infection or
– When available, the ECG may provide useful excessive intake of potassium in food or medications
information – Patients with hypoaldosteronism or Addison disease
are at risk for hyperkalemia because of a lack of
aldosterone
– Lack of aldosterone activity at the nephron causes – The nurse must caution patients to use salt substitutes
inadequate sodium and water reabsorption into the sparingly if they are taking other supplementary forms
bloodstream and inadequate excretion of potassium in of potassium or potassium-conserving diuretics.
the urine. Therefore, deficient adrenal hormones lead to o In addition, potassium-conserving diuretics,
sodium loss and potassium retention potassium supplements, and salt substitutes
should not be given to patients with kidney injury

B. CLINICAL MANIFESTATION
– The most important consequence of hyperkalemia is its
effect on the myocardium.
– Cardiac effects of elevated serum potassium are
usually not significant when the level is less than 7
mEq/L (7 mmol/L); however, they are almost always
present when the level is 8 mEq/L (8 mmol/L) or
greater.
– As the plasma potassium level rises, disturbances in
cardiac conduction occur.
– Ventricular arrhythmias and cardiac arrest may occur

C. ASSESSMENT AND DIAGNOSTIC FINDINGS

– Serum potassium levels and ECG changes are crucial
to the diagnosis of hyperkalemia, as discussed
previously.
– ABG analysis may reveal either a metabolic or a
respiratory acidosis.
– These are discussed further in the section on acid–
base disturbances in this chapter. Correcting the
acidosis helps correct the hyperkalemia.

D. NURSING MANAGEMENT
– Patients at risk for potassium excess (e.g., those with
kidney disease) need to be identified and closely
monitored for signs of hyperkalemia.
– The nurse monitors I&O and observes for signs of
muscle weakness and arrhythmias.
o When measuring vital signs, an apical pulse
should be taken.
– The presence of paresthesias and GI symptoms such
as nausea and intestinal cramping should be noted.
– Serum potassium levels, as well as BUN, serum
creatinine, serum glucose, and ABG values, should be
monitored for patients at risk for developing
hyperkalemia

PREVENTING HYPERKALEMIA
– Measures should be taken to prevent hyperkalemia in
patients at risk, when possible, by encouraging the
patient to adhere to the prescribed potassium
restriction.
– Potassium-rich foods to be avoided include many fruits
and vegetables, legumes, whole-grain breads, lean
meat, milk, eggs, coffee, tea, and cocoa.
o Conversely, foods with minimal potassium
content include butter, margarine, cranberry
juice or sauce, ginger ale, gumdrops or jelly
beans, hard candy, root beer, sugar, and honey.
Labels of cola beverages must be checked
carefully because some are high in potassium
and some are not

CORRECTING HYPERKALEMIA
– It is possible to exceed the tolerance for potassium if
given rapidly by the IV route. Therefore, careful
monitoring is necessary when administering potassium
solutions.
– Particular attention is paid to the solution’s
concentration and rate of administration. IV
administration should only be via an infusion pump
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
ALLERGIES
FABELLAR, AIDON JOSH B.
MR. ALLAN PAULO BLAQUERA, RN

ALLERGY
– Allergic diseases occur as a result of abnormal antigen- TYPE I: IMMEDIATE
antibody responses. • With an immediate or type I allergic response, IgE
– Symptoms can be chronic and minor, such as those receptor sites attached to the surface of mast cells bind
that occur with seasonal rhinitis, or acute and severe, to IgE antibodies responding to the presence of an
as in anaphylactic reactions. antigen.
– Allergy occurs when a person reacts to substances in • Mast cells are specialized cells found in the lining of
the environment that are harmless to most people blood vessels in the lungs and in connective tissue, the
o These substances are known as allergens and mucous membranes, and the skin.
are found in dust mites, pets, pollen, insects,
• IgE triggers mast cells to release intracellular granules.
ticks, molds, food, and some medications
These contain histamine, leukotrienes, a slow-reacting
– Atopy is the genetic tendency to develop allergic
substance of anaphylaxis (SRS-A) and chemotactic
diseases. When atopic people are exposed to allergens
substances 9substances to draw leukocytes into the
they can develop an immune reaction that leads to
area)
allergic inflammation. This can cause symptoms in the:
• Histamine and leukotrienes cause peripheral
o Nose and/or eyes, resulting in allergic rhinitis
vasodilation and permeability of blood vessels
(hay fever) and/or conjunctivitis
o This leads to lowered blood pressure and
o Skin resulting in eczema or hives (urticaria)
edema
o Lungs resulting in asthma
o SRS-A causes extreme bronchial constriction.
o If not treated immediately by an injection of
epinephrine to dilate the airway and initiate
vessel vasoconstriction, this “anaphylactic
reaction” can lead to shock and death
• Anaphylactic reactions can be caused by stinging insect
bites, exposure to certain drugs, or latex; however, food
allergy is the most common cause of anaphylaxis seen
in hospital emergency rooms in both children and adults

TYPE II: CYTOTOXIC RESPONSE

• Cells are detected as foreign and immunoglobulins
directly attack and destroy them without harming
surrounding tissue.
• Foreign red blood cells that are introduced to an Rh-
negative woman by an Rh-positive fetus are destroyed
by this process (Rh Incompatibility)

TYPE III: IMMUNE COMPLEX

• A type III response is an IgG- or IgE-mediated antigen–
antibody complex reaction that involves complement
and initiates the inflammatory response.
• Complement reactions that persist beyond the usual
inhibition may serve as the basis for many autoimmune
illnesses and serum sickness.

TYPE IV: CELL-MEDIATED HYPERSENSITIVITY

I. HYPERSENSITIVITY • In a delayed hypersensitivity response, T lymphocytes
• The underlying cause of all allergic disorders appears react with antigens and release lymphokines to call
to be an excessive antigen-antibody response when the macrophages into the area. An inflammatory response
invading organism is an allergen rather than an occurs that helps to destroy the foreign tissue.
immunogen • Contact dermatitis is another example of a delayed
o Termed a type I response or a hypersensitivity hypersensitivity response.
response when it happens immediately • Certain substances, such as cosmetics, household
products, or cured leather, alter the protein of skin cells
so that the skin cells become an antigen or the foreign
substance combines with the protein (hapten
formation) to become an antigenic protein.
• Lymphocytes and macrophages infiltrate the area and
attempt to destroy the offending protein. Redness and
vesicles develop, and pruritus may be intense.
 A. ASSESSMENT OF ALLERGIES IN CHILDREN
• History taking PHARMACOLOGIC THERAPY
• Laboratory testing • Intranasal steroids can be used prophylactically to
prevent inflammation
SKIN TESTING • Second- and third-generation antihistamines, such
• Skin testing is done to determine potential triggers for as cetirizine (Zyrtec) and loratadine (Claritin), cause
atopic symptoms by detecting the presence of IgE to little drowsiness yet effectively block histamine release
specific allergens and, as a result, control itching, sneezing, and
• When an allergen is introduced into the child’s skin and rhinorrhea
the child is sensitive to that allergen, a wheal (a small, • Decongestants such as pseudoephedrine (Sufaded)
raised bump that looks like a mosquito bite) and flare decrease nasal edema and can help enlarge breathing
(erythema that surrounds the wheal) response will space
appear at the site of the test from the release of
histamine by the local mast cells. IMMUNOTHERAPY OR HYPOSENSITIZATION
o Because this reaction appears quickly, the test • This is done when the child’s allergy symptoms cannot
should be read within 15 to 20 minutes. be controlled by avoidance of an allergen or
• Scratch, prick, or puncture skin testing is done to detect conventional drug therapy
sensitivity to aeroallergens, foods, stinging insects, and • Immunotherapy works by increasing the plasma
some drugs. concentration of IgG antibodies, which then act to
• Skin testing is done by placing a drop of allergen prevent or block IgE antibodies from coming in contact
solution on the skin of the upper back of volar aspect of with an allergens
the arm and then scratching/pricking or puncturing • This is generally continued for 3 to 5 years because the
through the drop of liquid with a sharp device (needle, longer it is used, the longer the period of relief from
lancet, or multihead device) symptoms occur after it is stopped
• In order to be valid, both a positive (histamine) and • It may also prevent a mild atopic disorder such as
negative (saline) control must be included in the panel allergic rhinitis from turning into a severe atopic
tested disorder such as asthma
o Average diameter of the negative control = less
than 3 mm COMMON ALLERGIC REACTIONS
o Average diameter of the positive control = at
least 3 mm larger than the negative control for II. ANAPHYLACTIC SHOCK
the testing to be interpreted • Anaphylactic shock is an immediate, life-threatening,
type I hypersensitivity reaction that occurs after
• Intracutaneous testing to allergens is done when a exposure to an allergen in a previously sensitized child.
sensitivity to aeroallergens, some drugs (primarily • Anaphylaxis can be caused by exposure to foods such
penicillin), or stinging insects is suspected but not as milk, egg, peanut, and tree nuts; stinging insects
confirmed by prick/puncture/scratch skin tests. including yellow jackets, honeybees, paper wasps,
o Intracutaneous testing is done by injecting a hornets, and fire ants; certain drugs, primarily
small amount of a solution of allergen below the antibiotics, nonsteroidal anti-inflammatory drugs
epidermis of the skin of the forearm or back. (NSAIDs), and neuromuscular blocking agents; and
o The forearm is usually preferred to allow for the latex.
application of torniquet if a system reaction
occurs A. ASSESSMENT OF ANAPHYLAXIS
o This is never done with food allergens because Symptoms of anaphylaxis may include:
of the potential for the intracutaneous testing to • Breathing: wheezing, shortness of breath, throat
cause an anaphylactic reaction tightness, cough, hoarse voice, chest pain/tightness,
• With all forms of skin testing, if the child is sensitive to trouble swallowing, itchy mouth/throat, nasal
the test solution, a wheal and flare will occur at the test stuffiness/congestion
site • Circulation: pale/blue color, low pulse, dizziness, light-
• The size of the reaction is then measured and graded headedness/passing out, low blood pressure, shock,
as 1+ to 4+ or as slight, moderate, or marked response loss of consciousness
in comparison to the wheal and flare response to the • Skin: hives, swelling, itch, warmth, redness, rash
positive control. • Stomach: nausea, pain/cramps, vomiting, diarrhea
• Always have a syringe filled with 0.3 ml epinephrine • Other: anxiety, feeling or impending doom,
(Adrenalin) 1:1,000 on hand to counteract an itchy/red/watery eyes, headache, cramping of the
unexpected anaphylactic reaction from skin testing uterus

B. THERAPEUTIC MANAGEMENT B. THERAPEUTIC MANAGEMENT OF ANAPHYLAXIS

• Reducing the child’s exposure to the allergen is • Exposure to certain food, stinging insects,
possible when the offending allergen is a drug, food, or medications, and latex are the most common triggers
irritant of anaphylaxis
• Epinephrine injected intramuscularly is the standard
ENVIRONMENTAL CONTROL of care for the treatment of anaphylaxis regardless of
• Involves limiting exposure to allergens in a child’s the cause
environment o This reduces the risk of prolonged
• help parents understand that goal of environmental hospitalization and death
controls measures are to decrease exposure to allergic o For maximum effectiveness, if anaphylaxis
triggers and reduce their child’s symptoms and follows an injection or an insect sting, inject the
decrease the need for medications or immunotherapy epinephrine into the vastus lateralis muscle of
the thigh or the unaffected arm
o The vasoconstrictor effects of epinephrine
prevent/relieve airway edema, hypotension,
 and shock and the beta-agonist effects
increase the effectiveness of cardiac
contractions and lead to bronchodilation

III. URTICARIA AND ANGIOEDEMA

URTICARIA
• Urticaria or hives refer to macular wheels surrounded
by erythema arising from the chorion layer of skin; they
are intensely pruritic (often described as having a
burning sensation)
o Hives may occur so closely together that they
end to coalese (blend together)
o Dilatation of capillaries and venules with
increased permeability occurs around the
lesions ATOPIC DISORDERS
o The cause of urticaria is a type I or immediate • Individuals with atopic disease are prone to all types of
hypersensitivity reaction created by the release allergic responses
of histamine from an antibody-antigen reaction, • Three disorder occur most frequently:
similar to but of lesser intensity than anaphylaxis o Allergic rhinitis
o In chronic urticaria, it is possible that no o Eczema (atopic dermatitis)
causative allergen can be found o Asthma
• The gene responsible for an immune response is
located near the human leukocyte antigen that is
responsible for graft rejections

IV. ALLERGIC RHINITIS

• This is associated with an IgE-mediated inflammatory
response to allergen exposure
• A risk factor for the development of asthma
• Inflammation of the nasal membranes that is
characterized by sneezing, nasal congestion, nasal
itching, and rhinorrhea, in any combination

A. ASSESSMENT
Common symptoms of allergic rhinitis include:
• Congestion
ANGIOEDEMA • Sneezing
• Angioedema is edema of the skin and subcutaneous • Nasal engorgement
tissue • Profuse watery nasal discharge
o This occurs most frequently on the eyelids,
hands, feet, genitalia, and lips – areas where ® The mucous membrane of the nose is generally paler
skin is loosely bound by subcutaneous tissue than normal
o It is not dependent, generally asymmetrically o It may be edematous, adding to nasal
distributed and usually occurs in conjunction congestion
with urticaria ® The eyes tend to water
o With severe angioedema, the larynx may be o The conjunctivae may be pruritic, often with a
involved distinctive pebbly appearance called
§ This may lead to airway obstruction and cobblestoning
subsequently, asphyxiation and death ® Children constantly rub their noses in an upward
motion, termed an “allergic salute”
® Allergens that most frequently cause urticaria and o Over a long period, rubbing the nose this way
angioedema includes: leads to a horizontal crease across the tip of the
• Drugs nose, called an allergic crease or Dennie line
• Foods ® The congestion in the nose, there tends to be back
• Insect stings pressure to the blood circulation around the eye orbit,
® Immediate therapy for urticaria or angioedema is an which leads to blackened areas under the eyes, termed
intramuscular epinephrine injection or the “allergic shiners”
administration of an oral antihistamine ® Triggers that usually cause allergic rhinitis:
o Pollen
o Molds
o Irritants rather than foods or drugs

However, with an upper respiratory infection, the mucous

membrane of the nose is more apt to be reddened than pale
and the secretions draining from the nose are apt to be thick
white or yellow rather than the thin, watery secretions of
allergic rhinitis. With an upper respiratory infection, a sore
throat and cervical adenopathy may also be present,
whereas these rarely accompany allergic rhinitis.

B. THERAPEUTIC MANAGEMENT
• Allergic rhinitis is managed by a three-pronged • The vesicles rupture and exude yellow, sticky
program: secretions that form crusts on the skin as they dry
o Avoidance of offending allergens o Because the lesions are extremely pruritic, the
o Use of pharmacologic agents (antihistamines, child scratches and further irritates the lesions,
leukotriene inhibitors, or corticosteroids) causing linear excoriations
o Immunotherapy • Secondary infections of open lesions may then occur
• If the child’s symptoms are increasing in intensity, if o If secondary infection occurs, the infant may
there is associated lower respiratory tract involvement, have a low grade fever and pus-filled lesions,
or if the condition interferes with activities in which the and local lymph nodes may be enlarged
child wants to participate, the child needs testing and • As the infected lesions heal, the skin becomes
treatment. depigmented and lichenified (shiny), and dry, flaky
scale form
• Infants usually present with rash on the face, neck, and
extensor surfaces

• Those children with minor symptoms can be managed

by environmental control and medications such as
antihistamines and/or intranasal steroids to reduce B. THEPAPEUTIC MANAGEMENT
symptoms. • Reducing the amount of allergen exposure (if allergens
o It is helpful if children and parents choose an can be identified)
antihistamine that causes the least amount of • Most likely foods to which infants are allergic:
drowsiness so the medication does not interfere o Milk
with schoolwork or, if an adolescent, with safe o Eggs
driving. o Peanuts
• Reducing pruritis so children do not irritate lesions and
V. PERENNIAL ALLGERIC RHINITIS cause secondary infections by scratching
• Allergic rhinitis becomes perennial (year round) when o Microbial colonization and superinfection
the allergen is one that is present in the environment increase pruritus contributing to the scratch-itch-
year round, such as house dust mites or pet hair. scratch cycle and can justify additional
o Because the agent that causes perennial allergic antimicrobial treatment.
rhinitis is often something in the house, • Hydrating the skin by bathing or applying we dressings
environmental control as well as SLIT can play a (moistened with tap water or Burow’s solution) for 15 to
big role in control of the allergic symptoms 20 minutes, followed by the application of a barrier to
• Defined clinically as an inflammatory condition of the seal in the moisture
nose characterized by nasal obstruction, sneezing, • In develop frequent secondary infections, weekly use of
itching, or rhinorrhea, occurring for an hour or more on dilute bleach baths can be very effective
most days throughout the year. • Antihistamine can be useful to reduce itching
• Low potency steroids can be used for maintenance
VI. ATOPIC DERMATITIS (INFANTILE ECZEMA) with intermittent and high-dose topical steroids for
• This is a highly pruritic, chronic inflammatory skin exacerbations
disease that is often the first manifestation of allergic • Intermittent and high dose topical steroids should
disease not be applied to face, eyelids, or genitalia
• A complex inflammatory process that involves an • Topical calcineurin inhibitors tacrolimus and
epidermal barrier defect pimecrolimus are also useful in atopic dermatitis
• Food allergy is a major trigger of atopic dermatitis in management
infants • Relapsing atopic dermatitis and severe refractory cases
• It is a long-term (chronic) skin condition. It causes dry, of atopic dermatitis may require long-term, anti-
itchy skin. It’s a very common condition in babies and inflammatory therapy with intermittent use of systemic
children. It usually first appears between ages 3 and 6 anti-inflammatory or immunosuppressive treatment
months.
• It involves intense pruritus and associated scratching VII. ATOPIC DERMATITIS IN OLDER CHILDREN
that disturbs sleep • Atopic dermatitis that occurs at later ages is prominent
• Sweating, heat, tight clothing, and contact irritants such on the flexor surface of the extremities and on the
as soap tend to increase the pruritis associated with dorsal surfaces of the wrists and ankles
eczema • It often occurs in the eyebrows; if the child scratches
the lesions, hair loss and scant eyebrows can result
• Depigmentation or hyperpigmentation is usually noticed
as lesions fade; lichenification can be marked

A. THERAPEUTIC MANAGEMENT
• Use only a prescription soap (or none at all) to prevent
skin drying
• Swimming in chlorinated pools may also help for those
who experience chronic secondary infections
• When children swim in chlorinated pools, encourage
them to shower well afterward to remove chlorine from
the skin as well as to apply a skin emollient and
moisturizer after the shower.
A. ASSESSMENT • After a period of activity in which sweating occurs, such
• Children develop popular and vesicular skin eruptions as gymnastics, suggest the child take a shower to
with surrounding erythema remove perspiration so this doesn’t irritate the skin.
• Avoiding tight clothing at the flexor portions of the • As with all allergies, nurses need to document contact
extremities is also important. allergies on health records so all healthcare providers
• Keeping the skin hydrated and identifying allergens and can be aware of them and guard against a reaction.
any psychological problems that are initiating an itch–
scratch cycle. DRUG AND FOOD ALLERGIES
• The application of hydrocortisones or phototherapy with
IX. DRUG ALLERGIES
ultraviolet light both can make a big difference in
• Reactions to drugs differ, it is important to be familiar
helping lesions improve.
with the differences between an allergic reaction, a
toxic reaction, or a known side effect to a drug
VIII. CONTACT DERMATITIS
• This is an example of a delayed or type IV • A toxic reaction is one that occurs when a child has
received too much of a drug
hypersensitivity response
• Side effects of drugs are those that are known to occur
• It is a reaction to skin contact with an allergen (a
in addition to a therapeutic effect
substance irritating to the child only with prior
sensitization) • A drug itself may not be an allergen, but when the drug
combines with body protein, it becomes an allergen,
• The first reaction is generally erythema, followed by
which is why allergic responses occur not with initial
the development of intensely pruritic papules and then
administration of a drug but only after the protein
vesicles
interaction (hapten formation of sensitivity) has
• The allergen causing the irritation is often suggested by
occurred
the part of the child’s body that is affected
• Skin manifestations seen frequently include:
o Dermatitis from a diaper-washing compound
o Urticaria
appears in the diaper area
o Angioedema
o Allergy to cosmetic appears on the face
o Allergic contact dermatitis
o Oozing at the site of pierced ears suggests an
o Flushing
allergy to the nicked used in earring posts
o Pruritis
o Poison ivy appears on the hands and arms
o Purpura
where the child brushed against the plant
o Children who have repeated surgeries such as • Respiratory symptoms include:
those with spina bifida are at high risk of o Wheezing
developing allergies to latex and will have o Rhinitis
lesions where the latex touches them • Thrombocytopenia and hemolytic anemia may develop
• Anaphylactic shock may occur
• Injectable drugs that are most frequently involved in
allergic reactions are cephalosporins and penicillin
• If urticaria, an antihistamine such as diphenhydramine
hydrochloride (Benadryl) may be helpful in relieving the
symptoms.
o If anaphylaxis results, the treatment would be
the administration of epinephrine.

X. FOOD ALLERGIES
• Food allergies are an abnormal immune response
caused by an exposure to a particular food protein.
• They can be IgE-mediated, cell-mediated, or mixed
reactions, although IgE-mediated (type I
hypersensitivity) reactions account for most food
reactions
A. ASSESSMENT • Symptoms of food allergies vary greatly among children
• Patch testing may be used to identify contact but cutaneous reactions to foods including:
dermatitis allergens. o Urticaria
o Should not be taking a corticosteroid at the o Angioedema
time of patch testing because these drugs o Flushing
reduce delayed hypersensitivity reactions. o Pruritus
o May continue taking antihistamines or
• Type I hypersensitivity reactions can manifest
sympathomimetic drugs because these do not
themselves only seconds after an offending food is
interfere with this testing eaten
• After 48 hours, the patches used for testing are • Most common foods that cause immediate allergy
removed and the reactions are graded 1+ to 4+, the
symptoms include:
same as in regular skin testing.
o Peanut
o Egg whites
B. THERAPEUTIC MANAGEMENT o Milk
• Removing the identified allergen from the child’s o Wheat
environment o Soy
• Dressings moistened with water, saline, or Burrow’s o Seafood
solution relieve itching o Tree nuts
• Calamine and Caladryl lotions are also generally • Chicken with milk and egg allergy may be able to
effective tolerate baked good that contain milk and/or egg
• Hydrocortisone lotions or creams reduce itching and because the exposure to high heat destroys the
also promote healing conformational epitopes, about 70% of children with a
• Baths with baking soda or oatmeal in the water may be diagnosed milk or egg allergy tolerate those proteins
helpful if a large area of the body is involved. after they have been baked in foods such as muffins
and cakes
 C. ASSESSMENT
• Sensitization can occur as food protein cross the
placenta or via breast milk.
• For some children, the first “known” exposure to milk,
egg, or peanut causes an immediate type I response
such hives, swelling, and vomiting.
o These reactions can be anaphylactic

D. THERAPEUTIC MANAGEMENT
• The easiest treatment for a food allergy is to eliminate
offending foods from the child’s diet.
o This is difficult when the foods are great in
number or if, like milk, wheat, or eggs, are found
in many products
• Urge parents to become conscientious shoppers and
read labels carefully to be certain the foods they are
buying do not contain products to which their child is
sensitive.

XI. VACCINES
• Mild local reactions and fever after vaccinations are
common and do not contraindicate future doses.
• Anaphylactic reactions to vaccines are rare.
• Children who are egg allergic can and should receive
injectable influenza vaccine as well as the MMR
vaccine.
• The yellow fever vaccine requires special precautions
for children with egg allergy.

XII. MILK INTOLERANCE

• Milk is one of the leading causes of type I reactions to
foods. (not all milk reactions are IgE-mediated
reactions)
• Milk intolerance usually presents in infancy and is
typified by failure to gain weight, diarrhea, perhaps
vomiting, and abdominal pain.
o Because these symptoms also occur in
gastrointestinal disorders, infants with colic
(characterized by abdominal pain, no change in
stools, and no failure to gain weight), those with
lactase deficiency, or those with a gastroenteritis
infection (have nausea and vomiting) may be
incorrectly diagnosed as having a milk allergy.
• Most infants can tolerate breast milk, even if the mother
consumes milk in her diet.
o Supplementing with a hydrolyzed protein-
based formula usually decreases symptoms
dramatically.

XIII. PEANUT HYPERSENSITIVITY

• Adults who care for children who are food allergic to
peanut need to be very aware of this danger and need
anaphylaxis action plans and epinephrine auto-injectors
available at all times
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
DENGUE
BUENAVENTURA, NIÑO KAE C.
MR. ALLAN PAULO BLAQUERA, RN

o Mucosal bleeding
DENGUE o Difficulty breathing
– It is a viral infection transmitted to humans through the o Lethargy/restlessness
bite of infected mosquitoes o Postural hypotension
– This is caused by four similar viruses spread by o Liver enlargement
mosquitoes of the genus Aedes, which are common in o Progressive increase in hematocrit
tropical and subtropical areas worldwide
– When an Aedes mosquito bites a person who’s been B. CRITICAL PHASE
infected with a dengue virus, the mosquito can become – Begins at defervescence (abatement of a fever as
a carrier of the virus. If this mosquito bites someone indicated by a decrease in bodily temperature) and
else, that person can be infected with the dengue virus typically lasts 24-48 hours
and can then get sick with dengue fever. The virus can’t – Those with substantial plasma leakage can develop
spread directly from person to person severe dengue as a result of marked increase in
– In rare cases, dengue fever can lead to a more serious vascular permeability
form of the disease called dengue hemorrhaging o Patients with severe plasma leakage may have
fever (DHF). It can be life-threatening and needs to be pleural effusions, ascites, hypoproteinemia,
treated right away. or hemoconcentration
– People can be infected with DENV up to four times – Physiologic compensatory mechanisms maintain
because there are four dengue virus adequate circulation which narrows pulse pressure as
diastolic blood pressure increases
SIGNS AND SYMPTOMS – Patients can also develop severe hemorrhagic
Common signs and symptoms of dengue fever include: manifestations, including hematemesis, bloody stool,
o High fever (as high as 40ºC) or menorrhagia, especially if they have been in
o Pain behind the eyes and in the joints, muscles prolonged shock.
and/or bones – Uncommon manifestations include hepatitis,
o Severe headache myocarditis, pancreatitis, and encephalitis.
o Rash over most of the body
o Mild bleeding from the nose or gums C. CONVALESCENT PHASE
o Bruising easily – As plasma leakage subsides, the patient enters the
convalescent phase and begins to reabsorb
• After the fever eases, other symptoms can get work and extravasated intravenous fluids and pleural and
may cause more severe bleeding abdominal effusions.
• Gastrointestinal problems like: – As a patient’s well-being improves, hemodynamic
o Nausea status stabilizes (although he or she may manifest
o Vomiting bradycardia), and diuresis ensues.
o Severe abdominal pain o The patient’s hematocrit stabilizes or may fall
• Respiratory problems: because of the dilutional effect of the
o Difficulty breathing reabsorbed fluid, and the white cell count usually
• Dehydration, heavy bleeding, and a rapid-drop in blood starts to rise, followed by a recovery of platelet
pressure (shock) can follow if DHF goes untreated. count.
– The convalescent-phase rash may desquamate and be
Dengue begins abruptly after a typical incubation period of pruritic.
5–7 days, and the course follows 3 phases: febrile, critical,
and convalescent. DIAGNOSIS

DENGUE VIRUS ANTIGEN DETECTION (NS1)

A. FEBRILE PHASE
– Fever typically lasts 2-7 days and can be biphasic • NS1 tests detect the non-structural protein NS1 of
(have two phases) dengue virus. This protein is secreted into the blood
– Signs and symptoms: during dengue infection.
o Severe headache • NS1 is detectable during the acute phase of dengue
o Retro-orbital eye pain virus infections. NS1 tests can be as sensitive as
o Muscle, joint, and bone pain molecular tests during the first 0-7 days of symptoms.
o Macular or maculopapular rash After day 7, NS1 tests are not recommended.
o Minor hemorrhagic manifestations:
§ Petechia (pinpoint, round spots that TREATMENT
appear on the skin as a result of • Mild cases are managed with lots of fluids to prevent
bleeding) dehydration and getting plenty of rest.
§ Ecchymosis (bruise) • Pain relievers with acetaminophen can ease the
§ Purpura headaches and pain from dengue fever.
§ Epistaxis (nosebleed) o Pain relievers with aspirin or ibuprofen should be
§ Bleeding gums avoided, as they can make bleeding more likely.
§ Hematuria (blood in the urine) • To treat severe cases of dengue fever at a hospital,
§ Positive tourniquet result doctors will give intravenous (IV) fluids and
– Some patients have injected oropharynx and facial electrolytes (salts) to replace those lost through
erythema in the first 24-48 hours onset vomiting or diarrhea.
– Warning signs: • When started early, this is usually enough to effectively
o Persistent vomiting treat the disease. In more advanced cases, doctors
o Severe abdominal pain may have to do a blood transfusion.
o Fluid accumulation
 PREVENTION
• Use screens on doors and windows, and promptly
repair broken or damaged screens. Keep unscreened
doors and windows shut.
• Have kids wear long-sleeved shirts, long pants, shoes,
and socks when they go outside, and use mosquito
netting over their beds at night.
• Use insect repellent as directed on kids.
• Limit the amount of time kids spend outside during the
day, especially in the hours around dawn and dusk,
when mosquitoes are most active.
• Don't give mosquitoes places to breed. They lay their
eggs in water, so get rid of standing water in things like
containers and discarded tires, and be sure to change
the water in birdbaths, dog bowls, and flower vases at
least once a week.

NURSING MANAGEMENT
Assessment of a patient with DHF should include:
• Evaluation of the patient's heart rate, temperature, and
blood pressure.
• Evaluation of capillary refill, skin color and pulse
pressure.
• Assessment of evidence of bleeding in the skin and
other sites.
• Assessment of increased capillary permeability.
• Measurement and assessment of the urine output.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
STREPTOCOCCAL INFECTIONS
CALIGUIRAN, MARIA ERIKA C.
MR. ALLAN PAULO BLAQUERA, RN

o Nursing management: The nurse should

STREPTOCOCCAL INFECTIONS stress fluid intake with cool, nonacidic
– Streptococci, which are gram-positive organisms, are fluids and soft, nonirritating foods.
found normally in the respiratory, alimentary, and
female genital tracts. B. RHEUMATIC FEVER AND GLOMERULONEPHRITIS
– S. pyogenes or Lancefield group A streptococcus are – Rheumatic fever is an inflammatory condition that can
responsible for mild infections like impetigo, tonsillitis, develop if strep throat, scarlet fever, and strep skin
or scarlet fever; however, they can also produce infections are not treated properly.
severe infections such as toxic shock syndrome or – conditions that may result as an autoimmune response
necrotizing fasciitis to streptococci
– S. pyogenes (β-hemolytic streptococci, group A) is
responsible for strep throat and scarlet fever, and SIGNS AND SYMPTOMS
this is treated due to the risk of nonsuppurative • congestive heart failure
complications of rheumatic fever and • chest pain
glomerulonephritis.
• shortness of breath
– A β-hemolytic, group B streptococcal infection can be
• fast heartbeat
contracted from vaginal secretions at birth; when
newborns become infected with these bacteria, • Fatigue (tiredness).
they can die from sepsis, pneumonia, or meningitis.

MANIFESTATIONS OF GROUP A STREPTOCOCCAL

INFECTIONS INCLUDE
• erysipelas,
• cellulitis,
• pneumonia,
• endocarditis,
• pericarditis,
• osteomyelitis,
• sepsis,
• bacteremia,
• and toxic shock syndrome

MANIFESTATION OF GROUP A STREPTOCOCCAL

MANAGEMENT
INFECTIONS
• Antibiotics. Penicillin or another antibiotic is
A. STREPTOCOCCAL PHARYNGEAL INFECTIONS typically prescribed to treat the strep bacteria.
– Pharyngeal infections are very common in patients of all After the first antibiotic treatment is fully finished, a
ages. They are typically associated with a sore and provider typically prescribes another course of
swollen throat that makes it difficult for the patient to antibiotics to prevent recurrence of rheumatic fever.
swallow. Preventive treatment will likely continue through age
21 or until a child completes a minimum five-year
SIGNS AND SYMPTOMS course of treatment, whichever is longer.
• sore throat People who have had heart inflammation during
• temperature greater than 100.4°F (38°C) rheumatic fever might need to continue preventive
• tonsillar exudates antibiotic treatment for 10 years or longer.
• and cervical adenopathy. • Anti-inflammatory drugs. Aspirin or naproxen
(Naprosyn, Naprelan, Anaprox DS) can help reduce
• Cough, coryza,
inflammation, fever and pain. If symptoms are
• diarrhea
severe or a child doesn't get better with anti-
inflammatory medicines, a corticosteroid might be
prescribed. Don't give a child aspirin unless a care
provider tells you to do so.
• Antiseizure drugs. Medications such as valproic
acid or carbamazepine (Carbatrol, Tegretol, others)
may be used to treat severe involuntary movements
caused by Sydenham chorea.
• A health care provider might recommend bed rest
for a child with rheumatic fever.
MANAGEMENT
• Children with infectious mononucleosis should be C. SCARLET FEVER
treated for pain and fever with acetaminophen or – Scarlet fever occurs most commonly in school-age
nonsteroidal anti-inflammatory agents. children, peaking in the 7- to 8-year-old age group
• The child should be encouraged to rest when fatigued, – The incidence is highest in temperate climates, and the
and all contact sports should be avoided for at least 4 disease occurs usually in late autumn, winter, and early
weeks after the onset of infection spring
• It can take 3 months for the child to return to his or her – Bacterial illness that develops in some people who
baseline fitness. have strep throat. Also known as scarlatina, scarlet
fever features a bright red rash that covers most of the
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
STREPTOCOCCAL INFECTIONS
CALIGUIRAN, MARIA ERIKA C.
MR. ALLAN PAULO BLAQUERA, RN

body. Scarlet fever almost always includes a sore throat

and a high fever.
 SIGNS AND SYMPTOMS • Cover your mouth and nose. Tell your child to cover
• Red rash. The rash looks like a sunburn and feels like the mouth and nose when coughing and sneezing to
sandpaper. It typically begins on the face or neck and prevent the potential spread of germs.
spreads to the trunk, arms and legs. Pushing on the D. IMPETIGO
reddened skin makes it turn pale. – Impetigo starts as a red, itchy sore. As it heals, a
• Red lines. The folds of skin around the groin, armpits, crusty, yellow or “honey-colored” scab forms over the
elbows, knees and neck usually become a deeper red sore. In general, impetigo is a mild infection that can
than the other areas with the rash. occur anywhere on the body.
• Flushed face. The face may appear flushed with a pale – It most often affects exposed skin, such as. Around the
ring around the mouth. nose and mouth.
– Causative agent: β-hemolytic streptococcus, group A
• Strawberry tongue. The tongue generally looks red
or S. aureus including MRSA
and bumpy, and it's often covered with a white coating
– Incubation period: 7 to 10 days for impetigo (AAP,
early in the disease.
2015)
• Fever of 100.4 F (38.0 C) or higher, often with chills
– Period of communicability: from outbreak of lesions
• Very sore and red throat, sometimes with white or until lesions are healed
yellowish patches – Mode of transmission: direct contact with lesions
• Difficulty swallowing – Immunity: none
• Enlarged glands in the neck (lymph nodes) that are – It is common to see several children in a family with
tender to the touch identical impetigo lesions because it is spread by direct
• Nausea or vomiting contact. An underlying scabies infection can cause
• Belly (abdominal) pain impetigo due to infection from scratching with nails
• Headache and body aches

MANAGEMENT
• Localized disease is treated with mupirocin (Bactroban)
ointment for 7 to 10 days (Box 43.6) or with retapamulin
(Altabax) for children over 9 months twice a day (bid) for
• Causative agent: β-hemolytic streptococci, group A 5 days. The use of oral antibiotic that cover both
• Incubation period: 2 to 5 days for streptococcal staphylococcus and streptococcus is reserved for
pharyngitis extensive impetigo.
• Period of communicability: greatest during acute
phase of respiratory illness; 1 to 7 days MUPIROCIN (BACTROBAN)
• Mode of transmission: direct contact from a person o Classification: Mupirocin is a topical antibiotic.
with the disease and large droplets, not fomites or Action: Mupirocin is used to treat impetigo caused
household pets by Staphylococcus aureus and Streptococcus
• Immunity: One episode of disease gives lasting pyogenes.
immunity to scarlet fever toxin. No vaccination is o Pregnancy Risk Category: B
o Dosage: small amount applied three times a day to
available.
the affected areas for 10 days duration
o Possible Adverse Effects: local irritation including
MANAGEMENT erythema, dry skin, pruritus, burning, stinging
• Children with scarlet fever usually recover without
sequela once penicillin is administered. Penicillin V is
the drug of choice RETAPAMULIN OINTMENT 1% (ALTABAX)
o Orally administered once a day amoxicillin at 50 o Classification: Retapamulin ointment 1% is a
mg/kg up to 1,200 mg as a daily dose for 10 topical antibiotic.
days o Action: Retapamulin ointment 1% is used to treat
• IM penicillin G benzathine is an alternative therapy if impetigo caused by S. aureus and S. pyogenes.
there is a history of noncompliance. o Pregnancy Risk Category: B
• Children may need an analgesic and antipyretic, such o Dosage: small amount applied twice times a day
as acetaminophen (Tylenol) or children’s ibuprofen to the affected areas for 5 days duration
(Motrin) for pain and fever. o Possible Adverse Effects: local irritation including
• Wash your hands. Show your child how to wash erythema, pruritus, burning, stinging
hands thoroughly with warm soapy water for at least 20
seconds. Alcohol-based hand sanitizer can be used if • Advise parents to wash the lesions with soap and water
soap and water are not available. and pat dry before applying ointment to soften crusts for
• Don't share dining utensils or food. As a rule, your better absorption.
child shouldn't share drinking glasses or eating utensils • Caution parents that causative organisms are infectious
with friends or classmates. This rule applies to sharing by direct contact. Instruct them to wash their own hands
food, too. before and after applying the ointment.
• Although the lesions may begin to improve before 10
days have elapsed, urge parents to continue to use the
ointment to ensure eradication of the causative bacteria.
• Instruct parents to use caution if applying the ointment
around the eyes because the ointment is irritating to the
eyes.

E. CAT-SCRATCH DISEASE
– Cat-scratch disease occurs most commonly in
preschool children because children at that age play
roughly with cats or pick them up and so receive
scratches. At the time, the child contracts the disease,
the cat does not appear ill.
– Causative agent: Bartonella henselae bacteria which is
slow growing
– Incubation period: usually 1 to 2 weeks with a range
of 7 to 60 days
– Period of communicability: unknown
– Mode of transmission: bite or scratch from more
commonly a kitten rather than a cat
– Immunity: one episode of disease gives lasting
immunity; no passive artificial immunity.

SIGNS AND SYMPTOMS

• a bump or blister at the bite or scratch site
• swollen lymph nodes near the bite or scratch site
• fatigue
• headaches
• a low-grade fever, which is above 98.6°F (37°C) but
below 100.4°F (37°C)
• body aches

MANAGEMENT
• Treatment is symptomatic, although azithromycin may
be prescribed to decrease the lymph node size.
• With more severe disease, treatment with
antimicrobials for several weeks will be initiated
• Children may need an analgesic to relieve pain from
the swollen lymph node.
• They can take an over-the-counter pain reliever to help
relieve pain and discomfort.
o Ibuprofen (two brands: Motrin, Advil) or
naproxen (one brand: Aleve) can help.
• Applying heat compresses to the affected area may
also help. If a lymph node is very large or painful, your
doctor may drain it to help relieve the pain.
• Antibiotics may be needed if your symptoms don’t go
away in a month or two. In rare cases, the infection can
travel to your bones, liver, or other organs.
• Wash hands carefully after handling your cat.
• Play gently with your cat so they don’t scratch or bite you.
• Don’t let your cat lick you, especially around the mouth,
nose, eyes, or open wounds.
• Control fleas to decrease the chance that your cat will
contract the bacteria.
• Don’t tease or provoke a cat.
• Avoid petting stray or feral cats.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
LEUKEMIAS
CORTEZ, ELLYZA L.
MR. ALLAN PAULO BLAQUERA, RN

LEUKEMIA – Often these patients have a fusion protein, the BCR-ABL

gene. This constitutively activates tyrosine kinase, the
mutation in this translocation between chromosome 9
and chromosome 22 causes a continuously on activation
of tyrosine kinase.

D. JUVENILE MYELOMONOCYTIC LEUKEMIA

(JMML)
– This is a rare cancer of the blood that affects young
children. JMML happens when types of white blood cells
called monocytes and myelocytes do not mature
normally. JMML can happen spontaneously (by chance)
or can be associated with other genetic disorders in
some children such as Down syndrome,
– Leukemia is the distorted and uncontrolled proliferation of neurofibromatosis, Li-Fraumeni syndrome, and Fanconi
WBCs (leukocytes) and is the most frequently occurring anemia.
type of cancer in children.
– Symptoms of leukemia can occur from a lack of normal Acute Lymphoblastic Leukemia and Acute Myeloid
bone marrow cell production or from accumulation of Leukemia are the most common type of leukemia in
malignant cells pediatrics. Chronic Myelogenous Leukemia is a slowly
– Acute Leukemia: clonal expansion of immature progressing blood and bone marrow disease that usually
precursors occurs during or after middle age, and rarely occurs in
– Chronic Leukemia: mature bone marrow components children. Juvenile Myelomonocytic Leukemia is rare as
that are then becoming clonal. well.

TYPES OF LEUKEMIA IN PEDIATRICS ASSESSMENT

A. ACUTE LYMPHOBLASTIC LEUKEMIA (ALL) • With ALL, because the bone marrow overproduces
– Acute lymphocytic leukemia (ALL) accounts for 75% of lymphocytes and therefore is unable to continue normal
leukemias and involves lymphoblasts (immature production of other blood components, the first
lymphocytes). symptoms of ALL in children usually are those
o Because of the rapid proliferation of so many associated with decreased RBC production
immature lymphocytes, the production of red (anemia) such as:
blood cells (RBCs) and platelets declines. o Pallor
o The abnormally proliferating cells are so o low-grade fever
immature that they may be identifiable as an o lethargy
immature “blast cell.” • A low thrombocyte (platelet) count will lead to
– The highest incidence of ALL is in children between 2 petechiae and bleeding from oral mucous membranes
and 6 years of age and cause easy bruising on arms and legs.
– Although it can be shown that leukemia in mice and cats • As the spleen and liver begin to enlarge from infiltration
is of viral origin, the cause of leukemia in children is of abnormal cells, abdominal pain, vomiting, and
unknown. anorexia occur.
– Radiation, exposure to chemicals, or genetic factors may • As abnormal lymphocytes invade the bone periosteum,
have some influence on the occurrence as children with the child experiences bone and joint pain.
Down syndrome are more likely to develop leukemia • Central nervous system (CNS) invasion leads to
than other children. symptoms such as headache or unsteady gait.
• On physical assessment, painless, generalized
B. ACUTE MYELOID LEUKEMIA (AML) swelling of lymph nodes is revealed. Laboratory
– Acute myeloid leukemia (AML) involves the over studies reveal an elevated leukocyte count with cells
proliferation of granulocytes (neutrophils, basophils, and almost stopped at the blast cell stage. The platelet
eosinophils). It is most often seen in adults and accounts count and hematocrit value will be low;
for only about 20% of all childhood leukemias. The • RBCs that are present are normocytic and
frequency of the disorder increases in late adolescence. normochromic (of normal size and color) but few in
– With AML, granulocytes grow so rapidly that they are number. A lumbar puncture may show evidence of blast
forced out into the bloodstream while still in the blast cells in the cerebrospinal fluid (CSF).
stage; these immature cells are not able to carry out • A bone marrow aspiration (performed at the iliac crest)
normal immune functions and put the child at risk for will be prescribed to identify the type of WBC involved,
infection. As with ALL, the over proliferation of which documents the type of leukemia.
granulocytes limits the production of RBCs and platelets.
– Children with Down syndrome have a 50-fold THERAPEUTIC MANAGEMENT
increase in their risk for AML. – Up to 95% of children with ALL will achieve a first
remission. If a child experiences a relapse, the chances
C. CHRONIC MYELOGENOUS LEUKEMIA (CML) of long-term survival are reduced, and bone marrow
– This is a myeloproliferative disorder characterized by transplantation may be required to achieve long-term
increased proliferation of the granulocytic cell line survival
without the loss of their capacity to differentiate.
Consequently, the peripheral blood cell profile shows an
increased number of granulocytes and their immature
precursors, including occasional blast cells.
 methotrexate to neutralize its action and protect normal
– For AML, the diagnosis is established by bone marrow cells from the effect of the drug.
aspiration and biopsy. After diagnosis, chemotherapy to
effect remission begins. Cytarabine (Ara-C), etoposide MAINTENANCE AND MONITORING
(VePesid), and daunorubicin (DaunoXome) make up the
drug regimen commonly used for therapy. It may take 1 – Maintenance chemotherapy aims to eliminate completely
to 2 months to reach a full remission. Bone marrow any remaining leukemic cells. Standard maintenance
transplantation may be attempted after the initial therapy includes a combination of daily mercaptopurine,
remission to ensure a sustained remission. weekly methotrexate, sporadic vincristine and
prednisone, and intrathecal methotrexate and may be
DISEASE CLASSIFICATION AND PROGNOSIS continued for 2 to 3 years. During the maintenance phase,
the child’s blood values must be monitored and are
– Leukemia is classified to define subgroups of cells and to usually in a safe range, allowing the child to return to most
predict the response to treatment. Blasts with B- of their pretreatment activities, including school and social
lymphocyte cell characteristics can be recognized by the activities. If there is serious bone marrow depression,
presence of immunoglobulin and antigen–antibody medication levels may be reduced.
receptors on their surfaces. B-lymphocyte cell types
account for about 85% of instances of ALL; the other 15% COMPLICATIONS
of children have T-lymphocyte cell involvement.
– Throughout therapy, the healthcare team and family need
CURE AS GOAL to be alert for complications of leukemia or of the therapy.
Among the problems seen long term are CNS, renal, and
– The goal of therapy for leukemia is complete cure, reproductive system disorders.
typically achieved with chemotherapeutic agents and
without radiation. Prognostic factors of the disease and CENTRAL NERVOUS SYSTEM INVOLVEMENT
presentation will be discussed with the family at
diagnosis. Adherence to therapy increases the chance of – If CNS involvement occurs, it can cause significant
cure and should be stressed when discussing home- complications. Blindness, hydrocephalus, and
administered chemotherapy. recurrent seizures are possible, although the meninges
– A chemotherapy program is aimed at, first, achieving a and the sixth and seventh cranial nerves are the
complete remission or absence of leukemia cells structures most often affected. With meningeal
(induction phase); second, preventing leukemia cells involvement, the child develops nuchal rigidity,
from invading or growing in the CNS (sanctuary or headache, irritability, and perhaps vomiting and
consolidation phase); third, administering delayed papilledema. A lumbar puncture will reveal the presence
intensive therapy; and fourth, maintaining the original of blast cells in the CSF. If these are discovered, the child
remission (maintenance phase). will be treated with radiation in conjunction with
– Chemotherapy in children is often administered by means intrathecal injections of chemotherapy. Always check that
of a central venous catheter or port because a child is not prescribed oral and IV methotrexate at the
administration of drugs into a major vessel helps prevent same time because some of the dose of intrathecal
irritation to the vessel walls. Central catheters are usually methotrexate will be absorbed systemically and could
in place for the duration of treatment and parents may lead to a toxic reaction. Insertion of silicon tubing into a
have maintenance responsibilities while the child as at cerebral ventricle and threading it under the scalp (an
home; for example, flushing with heparin or changing Ommaya reservoir) is sometimes employed and provides
dressings for external lines. Portacaths are inserted easy access to the CSF for sampling or injection without
below the skin and accessed with a needle when needed. the need for repeated lumbar punctures.
They do not require home maintenance and allow for the
greatest freedom between treatments. RENAL INVOLVEMENT
– The drug regimen frequently used to initiate a remission
includes vincristine, prednisone or dexamethasone, – Kidney involvement, resulting from invasion of leukemia
L-asparaginase, and doxorubicin given over a period cells or obstruction of renal tubules with uric acid crystals,
of 4 weeks. Because so many cells are destroyed by is another serious complication. The kidneys enlarge, and
chemotherapy. During rapid cell destruction, a high level their function will be impaired. The development of renal
of uric acid must be excreted by the kidneys during involvement or impairment may limit the use of
treatment. To prevent kidney damage, the child will be chemotherapeutic agents because the metabolites of
kept well hydrated or a drug such as allopurinol will be these can no longer be excreted effectively.
initiated to help reduce the formation of uric acid.
– Although a chemotherapy protocol will achieve disease TESTICULAR INVASION
remission in 95% of children, because many
chemotherapy drugs do not cross the blood–brain barrier – Males are at risk for testicular invasion with leukemic cells
in effective concentrations, leukemic cells in the CNS can which may not be destroyed with chemotherapy. Careful
continue to flourish. Intrathecal administration (injection physical exam of the testes is necessary throughout and
of methotrexate into the CSF by lumbar puncture) is after treatment to identify signs of testicular involvement.
instituted to eradicate this source of leukemic cells. If the testes are found to have leukemic invasion, local
Cranial radiation, once used extensively for this purpose, radiation is necessary for effective treatment. If a boy is
is rarely used today due to the learning disorders that may past puberty and is producing sperm, sperm banking may
result. be suggested before chemotherapy and radiation to
– The third phase of therapy (intensification phase) preserve sperm for reproduction later in life.
strengthens the assault against leukemic cells again
using chemotherapeutic agents such as vincristine,
prednisone, L-asparaginase, doxorubicin, and
methotrexate. A drug such as leucovorin (often called
leucovorin rescue) may be administered after systemic
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
URINARY TRACT INFECTIONS (UTI)
CALATI, KELLY KEITH JANN R.
MR. ALLAN PAULO BLAQUERA, RN

• Urine for culture can be collected using a clean-catch

URINARY TRACT INFECTIONS technique, suprapubic aspiration, or catheterization, so
– UTIs occur more often in girls than boys because the bacteria from the vulva or foreskin do not contaminate
urethra is shorter in girls, and because it is located close the sample and give a false result.
to the vagina and anus, vulvovaginitis or rectal bacteria • Suprapubic aspiration is generally limited to infants.
can easily spread to the urethra. Catheterization, also frightening and a potential source
– Urinary pathogens seem to enter the urinary tract most of infection, is limited in children of all ages.
often as an ascending infection from the perineum and • Urine obtained from suprapubic aspiration is generally
are gram-negative rods such as Escherichia coli. sterile, so any growth from this source is significant. A
– UTIs also occur as a health care–acquired infection in clean-catch urine specimen is said to be positive for
children who have urinary catheters. bacteriuria if the bacterial colony count is more than
100,000 per milliliter.
Management: o count of less than 10,000 per milliliter is
® Changing diapers frequently can help reduce the risk for considered a negative culture.
infection in infants. o count is between 10,000 and 100,000 per
® Girls should be taught early (when they are toilet-trained) milliliter or if the urine is positive for
to wipe themselves from front to back after voiding and proteinuria (which could happen because of the
defecating to avoid contaminating the urethra. presence of bacteria), the count is usually
repeated.
– It’s important that UTIs are treated so they do not • In addition to identifying the responsible organism,
damage the bladder lining and/or spread to involve the microscopic examination of the urine specimen may
kidneys (pyelonephritis) and cause permanent indicate the presence of red blood cells (hematuria)
damage. caused by bacterial irritation of the bladder mucosa.
– Girls who have one UTI should be thoughtfully assessed • The presence of either red or white blood cells or
and, if a second UTI occurs, should be referred to a bacteria tends to make urine more alkaline, so the pH
fellowship-trained pediatric urologist to determine of the sample will be elevated (>7)
whether any congenital urologic anomaly such as an
urethral stenosis or vesicoureteral reflux exists.
THERAPEUTIC MANAGEMENT
– Any male older than the age of 3 months who presents
- Oral administration of a broad-spectrum antibiotic such
with UTI should also be evaluated by a pediatric
as sulfamethoxazole-trimethoprim (Bactrim) or
urologist.
amoxicillin, or;
- an antibiotic specific to the causative organism that is
cultured
- Nitrofurantoin is also a good choice for UTIs because
it is a broad-spectrum antibiotic that concentrates in the
urine and can be used for both treatment and
prophylaxis.
- A child needs to drink a large quantity of fluid to
“flush” the infection out of the urinary tract, particularly if
a sulfa drug is prescribed because these can cause
urinary crystals in concentrated urine.
- Cranberry juice is often recommended as being highly
effective in acidifying urine and making it more resistant
to bacterial growth. In actual practice, little evidence of
its effectiveness exists, so water is the best choice;
- Fluids with artificial coloring and carbonation should be
avoided because they irritate the bladder and can
cause further discomfort.
If the child experiences moderate to severe pain on urination
that interferes with the ability to void, suggest the child sit in
a bathtub of warm water and void into the water. A mild
analgesic, such as acetaminophen

ASSESSMENT
• The typical symptoms that occur in older children or in
adults – pain on urination, frequency, burning, and
hematuria – may not be present in young children, so
UTI is suspected when a child has a fever with no
demonstrable cause on physical examination.
• If the infection is confined to the bladder (cystitis), the
child may have a low-grade fever, mild abdominal
pain, and day or nighttime enuresis.
• If the infection progresses to pyelonephritis, the
symptoms are generally more acute, with high fever,
abdominal or flank pain, vomiting, and malaise.
 NCM 109 – CARE OF MOTHER, CHILD, AT RISK OR WITH PROBLEMS (ACUTE & CHRONIC)
ACUTE GLOMERULITIS (AGN)
COLLADO, DIANA NICOLE D.
MR. ALLAN PAULO BLAQUERA, RN

ACUTE GLOMERULONEPHRITIS • History of a recent respiratory infection (within 7 to 14

days) or impetigo (within 3 weeks)
GLOMERULONEPHRITIS
o Impetigo – is a common contagious skin
– inflammation of the glomeruli of the kidney, may occur
infection. Bacteria like Staphylococcus aureus or
as a separate entity but usually occurs in children as an
Streptococcus pyogenes infect the outer layers
immune complex disease after infection with
of the skin, called the epidermis. The face, arms,
nephritogenic streptococci (most commonly subtypes of
and legs are most often affected.
group A beta- hemolytic streptococci) where
• All children who have had a “strep” throat, tonsillitis,
complement, a cascade of proteins activated by
otitis media, or impetigo caused by a streptococcal
antigen– antibody reactions, plugs or obstructs
infection, ideally, should have a urinalysis 2 weeks
glomeruli.
after the infection to evaluate that glomerulonephritis
– Immunoglobulin G (IgG) antibodies against streptococci
is not occurring.
can be detected in the bloodstream of children with
acute glomerulonephritis, proof the illness follows a • The disorder is announced by a sudden onset of
streptococcal infection hematuria and proteinuria
® Proteinuria
o Urinary sediment will contain white blood
cells, epithelial cells, and hyaline,
granular, and red blood cell casts
o A single specimen of urine will show 1+
to 4+ protein; a 24-hour urine specimen
may contain as much as 1g of protein
(normal urine = no protein)
® Hematuria
o Tea-colored, reddish-brown, or smoky
urine
o After these initial urine changes, the child
develops oliguria (pee less than usual;
<20 ml/hour or 400 ml/day)
o Specific gravity of urine becomes
elevated
o Hypertension from hypervolemia occurs
• The child may have:
® Abdominal pain
® A low-grade fever
® Edema in the face, hands, feet, and abdomen
® Anorexia
® Vomiting
® Headache
® Cardiac involvement:
o Orthopnea (shortness of breath or DOB
when lying down; relieved by sitting or
standing)
o Cardiac enlargement
o Enlarge liver
o Pulmonary edema
o A galloping heart rhythm
o Heart failure because of the difficulty in
managing the excessive plasma fluid
• Blood analysis will indicate a lowered blood protein
level (hypoalbuminemia) caused by a massive
proteinuria
• As the blood volume expands, a mild anemia will also
develop
• As in all inflammatory diseases, the erythrocyte
sedimentation rate will increase
o The glomeruli cannot filter properly,
concentration of urea, nonprotein nitrogen
(BUN), and creatinine in blood will increase
• If blood pressure reaches 160/100 mmHg as a part of
ASSESSMENT the expanding circulatory volume, encephalopathy
® It is most common in children between the ages of 5 may occur, with symptoms of:
and 10 years, the age group most susceptible to o Headache
streptococcal infections o Irritability
® Boys appear to develop the disease more often than o Seizures
girls; it occurs more often during the winter and spring, o Vomiting
as do pharyngeal streptococcal infections. o Coma or lethargy
o Transitory paralysis
® Symptoms are all caused by cerebral ischemia hands, feet and abdomen. In rare instances, nephrotic
(vasoconstriction of cerebral vessels that occurs to syndrome may cause a blood clot in a kidney blood
reduce cranial pressure) vessel.

THERAPEUTIC MANAGEMENT
• A course of antibiotics may be prescribed to be certain
all streptococci are removed from the child’s system
• If heart failure occurs, keeping the child in a semi-
fowler’s position, digitalization, and oxygen
administration are helpful
• If diastolic blood pressure rises to more than 90 mmHg,
antihypertensive therapy with an antihypertensive
such as labetalol will be prescribed
• Phosphate binders (aluminum hydroxide) to reduce
phosphate absorption in the GI tract
• Potassium-removing resin agent (sodium polystyrene
sulfonate [kayexalate]) may be necessary in children
who have rising phosphate and potassium levels
because the kidneys are unable to clear these from the
circulation
• A diet that restricts salts – may limit edema and
limiting protein take may reduce the amount of protein
lost in urine

INFECTIOUS DISEASE can directly or indirectly lead to

glomerulonephritis. These infections include:
• Post-streptococcal glomerulonephritis –
Glomerulonephritis may develop a week or two after
recovery from a strep throat infection or, rarely, a skin
infection caused by a streptococcal bacterium
(impetigo). Inflammation occurs when antibodies to
the bacteria build up in the glomeruli. Children are
more likely to develop post-streptococcal
glomerulonephritis than are adults, and they're also
more likely to recover quickly.
• Bacterial endocarditis – Bacterial endocarditis is an
infection of the inner lining of your heart's chambers
and valves. It isn't clear whether the inflammation in
the kidneys is the result of immune system activity
alone or other factors.
• Viral kidney infections – Viral infections of the
kidney, such as hepatitis B and hepatitis C, cause
inflammation of the glomeruli and other kidney
tissues.
• HIV – Infection with HIV, the virus that causes AIDS,
can lead to glomerulonephritis and progressive kidney
damage, even before the onset of AIDS.

COMPLICATIONS
• Acute kidney failure – Acute kidney failure is the
sudden, rapid decline in kidney function, often
associated with an infectious cause of
glomerulonephritis. The accumulation of waste and
fluids can be life-threatening if not treated promptly with
an artificial filtering machine (dialysis). The kidneys
often resume typical function after recovery.
• Chronic kidney disease – Persistent inflammation
results in long-term damage and declining function of
the kidneys. Chronic kidney disease is generally
defined as kidney damage or decreased function for
three or more months. Chronic kidney disease may
advance to end-stage kidney disease, which requires
either dialysis or a kidney transplant.
• High blood pressure – Damage to the glomeruli from
inflammation or scarring can lead to increased blood
pressure.
• Nephrotic syndrome – Nephrotic syndrome is a
condition in which there is too much blood protein in
urine and too little in the bloodstream. These proteins
play a role in regulating fluids and cholesterol levels. A
drop in blood proteins results in high cholesterol, high
blood pressure and swelling (edema) of the face,