Module No.

05
Date: 04.07.2022
Topic: Pediatric Illnesses

CUES/QUESTIONS/ NOTES
KEYWORDS

CONGENITAL HEART DISORDERS

CLASSIFICATION
Based on physical sign of cyanosis
Acyanotic Heart Disease  involves heart or circulatory
anomalies that moves blood from the arterial to the venous
system
 Oxygenated to unoxygenated blood
 Left-to-right shunts

Cyanotic Heart Disease  blood is shunted from venous to

arterial system as a result of abnormal communication between
the two systems
 Unoxygenated blood to oxygenated blood
 Right-to-left shunts

Four Classifications
1) Increased pulmonary blood flow – VSD, ASD, PDA
2) Obstruction to blood flow leaving the heart – pulmonary
stenosis, aortic stenosis, COA
3) Mixed blood flow (oxygenated and deoxygenated blood mixing
in the heart or great vessels) – TGA, truncus arteriosus
4) Decreased pulmonary blood flow – tricuspid atresia, TOF

Ventricular Septal Defect

 most common type of congenital cardiac disorder
 an opening is present in the sputum between the two
ventricles
 greater pressure on the left ventricle
 left to right shunt (acyanotic disorder)

Symptoms
 begin around 4-8wks of age
 easy fatigue
 loud, harsh pansystolic murmur at 3rd – 4th interspace
 palpable thrill

Dx
 Doppler of MRI  R ventricular hypertrophy, pulmonary
 artery dilatation
 ECG  R Ventricular Hypotrophy

Management
 Up to 85% close spontaneously
 Open-heart surgery before 2yo

Atrial Septal Defect

 Abnormal communication between the two atria
 Left to right shift (acyanotic effect)

Assessment
 Harsh systolic murmur over the 2nd-3rd interspace
 Fixed splitting – second heart sound auscultated as split
 Dx: Doppler – enlarged right side of the heart, increased
pulmonary circulation

Therapeutic Management
 Surgery to close the defect is done electively between 1-
3 y/o.
 Without closure  infectious endocarditis  heart
failure

Patent Ductus Arteriosus

 Ductus arteriosus - fetal structure that connects the
pulmonary artery to the aorta.
 Closure begins with first breath, usually complete between 7-
14 days of age; full closure may be up to 3 mos.
 Blood shunts from aorta to the pulmonary artery (acyanotic)
 blood returns to L atrium  L ventricle  aorta 
pulmonary artery.
 Increased pressure in the pulmonary circulation  R
ventricle hypertrophy and ineffective heart action

Assessment
 Twice as common in girls as boys.
 Wide pulse pressure
 Continuous “machinery murmur at the upper left
sternal border or under the left clavicle
 Echocardiography – visualization of the patent ductus.

Management
 IV indomethacin, ibuprofen, prostaglandin inhibitors.
 Cardiac catheterization
 Surgical intervention: ductal ligation via thoracotomy

Pulmonary Stenosis
  Narrowing of the pulmonary valve or the pulmonary artery
just distal to the valve.
 Accounts for 10% of congenital heart anomalies
 Narrowing creates obstruction  unable to empty the right
ventricle  R ventricular hypertrophy

Assessment
 Asymptomatic, or signs of mild R-sided heart failure
 If severe, cyanosis
 Systolic ejection murmur, grade IV or V crescendo-
 decrescendo loudest at left sternal border
 Echocardiography – R ventricle hypertrophy

Therapeutic Management
 Depends on the age and severity
 Balloon angioplasty via cardiac catheterization
 After the procedure, the child may always have a
residual heart murmur

Aortic Stenosis
 Stenosis or stricture of the aortic valve.
 Prevents blood from passing freely from L ventricle to the
aorta  increased pressure and L ventricle hypertrophy 
increased pressure in L atrium  back-pressure in pulmonary
veins  pulmonary edema

Assessment
 Generally asymptomatic, typical murmur heard loudest
in the second right interspace
 Thrill may be present – suprasternal notch
 If severe, decreased cardiac output evidenced by:
 Faint pulses
 Hypotension
 Tachycardia
 Inability to suck for long periods
 When child is active 🡪 chest pain, similar to angina
 ECG or echocardiography 🡪 L ventricular hypertrophy

Therapeutic Management
 Beta blocker or calcium channel blocker – reduce
hypertrophy before the defect is corrected
 Balloon valvuloplasty – surgical treatment of choice
 For severe defects 🡪 dividing the stenotic valve, or
dilating a constrictive aortic ring
 Artificial valve replacement

Coarctation of the Aorta (COA)

  Narrowing of the lumen of the aorta due to a constricting
band
 Occurs more frequently in boys than in girls.
 Results in increased BP in the heart and upper body,
decreased BP in lower body 🡪 BP in arms at least 20 mmHg
higher than in legs

Assessment
 Mild: absent palpable femoral pulses
 As child grows older 🡪 leg pain on exertion d/t
diminished blood supply
 Echocardiography, MRI, X-ray – L sided heart
enlargement
 Soft or moderately loud systolic murmur may or may
not be present

Therapeutic Management
 interventional angiography (balloon catheter)
 surgery: narrowed portion of the aorta is removed, new
ends are anastomosed
 subclavian artery graft
 infants: digoxin therapy, diuretics pre-op

Transposition of the Great Arteries

 aorta arises from right ventricle instead of the left
 blood enters from vena cava to r atrium  r ventricle 
aorta completely deoxygenated then returns by vena
cava
 pulmonary artery arises from left ventricle instead of the right
 blood enters from pulmonary vein  l atrium  l
ventricle  pulmonary artery
 creates two closed circulatory system
 this defect is incompatible with life
 may also occur along with ASD/VSD
 tends to occur in large newborns and more often in boys than
girls

Assessment
 Usually cyanotic at birth
 No murmur, or various murmurs in presence of other
defects
 Echocardiography  enlarge heart
 Cardiac catheterization  low O2 sat

Therapeutic Management
 If no septal defect: PGE1 to keep ductus arteriosus
patent
  Balloon atrial septal pull-through: open the foramen
ovale
 Surgical correction at 1 week to 3 months of age –
arterial switch procedure

Truncus Arteriosus
 Rare defect, approximately 1%
 One major artery or “trunk” arises from left and right
ventricles
 Usually with accompanying VSD
 Cyanotic and may have typical VSD murmur
 Repair – restructuring the common trunk to create separate
vessels
 May need a second surgical procedure as the graft inserted is
outgrown

Tricuspid Atresia
 Extremely serious disorder because the tricuspid valve is
completely closed
 No blood flow from right atrium to the right ventricle
 Instead, blood crosses patent foramen ovale into L atrium 
bypasses lungs and therefore oxygenation
 Oxygenation by shunt via PDA
 As long as foramen ovale and ductus arteriosus remain open,
the child can obtain adequate oxygenation, but eventually
they will close
 Surgery: construction of vena cava to pulmonary artery shunt
(Fontan procedure or Glenn Shunt baffle)

Tetralogy of Fallot
 Four anomalies:
 Pulmonary stenosis
 VSD (usually large)
 Dextroposition (overriding) of the aorta
 Hypertrophy of the right ventricle
 A number of children with this disorder show a deletion
abnormality of chromosome 22

Assessment
 Absent or minimal cyanosis immediately after birth, but
becomes cyanotic thereafter.
 Polycythemia
 If not corrected:
 Severe dyspnea
 Growth restriction
 Clubbing of the fingers
 Child assumes squatting or knee-chest position
  Loud harsh widely transmitted murmur or a soft,
scratchy,
 localized systolic murmur in the L 2nd, 3rd or 4th
parasternal interspace.
 Echocardiography, ECG – enlarged R side of the heart,
decrease in size of pulmonary artery, reduced blood
flow to the lungs
 Cardiac catheterization and angiography – definitive
evaluation
 CBC inc. Hgb, Hct, dec. O2 sat

Therapeutic Management
 Surgical correction at 1-2 years of age
 O2 administration
 To prevent hypercyanotic episodes
 Place the baby in knee-chest position
 MSO4
 To generally reduce symptom
 Propanolol
 To aid pulmonary artery dilation
 Blalock-Taussig procedure
 temporary or palliative, creates a shunt between
the aorta and the pulmonary artery (creating a
PDA)
 Brock procedure
 full repair

DISORDERS OF THE RESPIRATORY SYSTEM

Acute Nasopharyngitis (Common Cold)
 Incubation period: typically 2-3days
 Common infectious agents: rhinovirus, coxsackievirus, RSV,
adenovirus, and parainfluenza and influenza viruses

Assessment
 nasal congestion
 watery rhinitis
 low-grade fever (except for infants)
 cervical lymph nodes may be swollen and palpable
 may progress into a cough and/or sore throat
 infants may develop secondary symptoms such as
vomiting and diarrhea

Therapeutic Management
 There is no specific treatment for a common cold.
 Symptomatic management:
 Acetaminophen or ibuprofen for fever
 !!! Children below 18 years old must not be given
 ASA
 Saline nose drops or nasal spray for infants
 Guaifenesin – expectorant

Pharyngitis
 Infection and inflammation of the throat

Viral pharyngitis
 Causative agent: adenovirus
 Si/Sx: sore throat, fever, general malaise, erythema on in
back of pharynx and palatine arch, increased WBC
 Warm compress, gargle with warm water, WOF dehydration

Streptococcal pharyngitis
 Group A beta-hemolytic streptococcus
 All streptococcal infections must be taken seriously 🡪 can
lead to cardiac and kidney damage from the accompanying
autoimmune process
 Si/Sx: erythematous back of throat and palatine tonsils
(bright red), enlarged tonsils, white exudate in the tonsillar
crypts, high fever, extremely sore throat, difficulty
swallowing, lethargy, headache
 Throat culture: (+) Streptococcus bacteria

Management
 10-day course oral antibiotics:
 Pen G
 Clindamycin
 Cephalosporins or broad-spectrum macrolides – (+)
resistance
 Si/sx of acute glomerulonephritis (AGN) appear in 1-2
weeks
 Child may be asked to come back after 2 weeks for a
urine test

Tonsillitis
 Infection and inflammation of the palatine tonsils.
 “Adenitis” – infection and inflammation of the adenoid
(pharyngeal) tonsils

Assessment
 same symptoms as pharyngitis
 drooling – the throat is too sore for them to swallow
saliva
 swallowing described as swallowing bits of metal or
glass
 high fever, lethargy
  tonsillar tissue appears bright red and enlarged
 pus can be detected or expelled from the tonsillar crypts
 Adenoid: nasal quality of speech, mouth breathing,
difficulty hearing, halitosis and sleep apnea
 throat culture

Therapeutic Management
 Tonsillectomy – removal of the palatine tonsils
 Adenoidectomy – removal of the pharyngeal tonsils
 done once the child is well; if done while the infection is
active, might spread the pathogen and cause septicemia
 WOF si/sx of hemorrhage: a child may be swallowing
blood

Epistaxis
 Nosebleed

Causes
 trauma
 homes that lack humidification
 strenuous exercise
 tends to occur during respiratory illnesses
 associated with several systemic illnesses: rheumatic
fever, scarlet fever, measles, chickenpox

Management
 Keep in upright position with head tilted slightly forward
to minimize blood pressure in nasal vessels
 Apply pressure to the sides of the nose with your fingers
 Keep the child quiet or help stop crying
 Nasal pack – cold compress
 Epinephrine (1:1000)

Sinusitis
 Infection and inflammation of the sinuses
 Rare in children younger than 6 years of age 🡪 frontal sinuses
do not
 develop fully until age 6
 Si/sx: fever, purulent discharge, headache, tenderness over
the affected sinuses
 (+) nose and throat culture
 Management
 antipyretic
 analgesic
 antibiotic for specific organism
 Oxymetazoline hydrochloride – nasal drops or nasal
spray
Laryngitis
 Inflammation of the larynx
 May occur as complication of phrayngitis or from excessive
use of voice, shouting or loud cheering
 Si/sx: brassy, hoarse voice sounds or inability to make audible
voice sounds
 Management
 Sips of fluid – warm or cold, whichever feels best.
 Have the child rest the voice for at least 24 hours
 For infants, attend to their needs before they start
crying
 Older child – caution them not to speak; provide a
whiteboard or paper and pencil for communication

Croup (Laryngotracheobronchitis)
 inflammation of the larynx, trachea, and major bronchi
 Common causative agent: viral infection such as parainfluenza
virus; H. influenzae

Assessment
 Mild upper respiratory tract infection symptoms at
bedtime
 Temperature is normal or slightly elevated
 During the night, they develop a barking cough (croupy
cough), inspiratory stridor, and marked retractions
 They wake in extreme respiratory distress
 These severe symptoms typically last several hours and
then, except for a rattling cough, subside by morning.
Symptoms may recur the following night

Therapeutic Management
 Run the shower or hot tap to fill the room with steam
and keep the child inside until symptoms are relieved
 If not relieved, bring child to emergency department
 Corticosteroid or racemic epinephrine via nebulizer
 IV therapy; monitor I&O and urine specific gravity

Aspiration
 Inhalation of a foreign object into the airway
 Occurs most frequently in infants or toddlers
 Initial reaction is choking, and hard, forceful coughing 🡪 can
dislodge the object
 Cough with no sound 🡪 airway is obstructed; intervention is
necessary
 subdiaphragmatic abdominal thrusts
 for infants, use back thrusts
Influenza
 Inflammation and infection of the major airways
 Caused by the orthomyxovirus influenza type A, B, or C
 Si/sx: cough, fever, fatigue, aching pains, a sore throat, and
often accompanying GI symptoms such as vomiting or
diarrhea.
 Management
 antipyretics – acetaminophen (Tylenol)
 Oseltamivir (TamiFlu) – children over 1 year old
 Flu vaccine

Bronchitis
 Inflammation of the major bronchi and trachea

Assessment
 mild URTI for 1-2 days  fever and dry, hacking cough
(hoarse and mildly productive in older children)
 cough is serious enough to wake a child from sleep
 si/sx may last a week, full recovery up to 2 weeks
 On auscultation, rhonchi and coarse crackles
 CXR: diffuse alveolar hyperinflation and some markings
in the hilus of the lungs

Therapeutic Management
 Therapy is aimed at relieving respiratory symptoms,
reducing fever, and maintaining adequate hydration
 Antibiotics – bacterial infections
 Expectorants

Respiratory Syncytial Virus Bronchiolitis

 RSV – pathogenic RNA virus that is most common cause of
bronchiolitis in young children

Si/sx
 mild URTI that quickly extends to bronchioles
 Infant quickly becomes lethargic and possibly cyanotic
 Dehydration
 Resp. distress – nasal flaring, retractions, grunting, rales,
 wheezing noted on auscultation
 !!! Monitor for apnea

Management
 Supportive therapy
 Supplemental oxygen
 Hydration
 Life-threatening apnea may need mechanical ventilation
  Ribavirin
 Isolate infants with RSV

Asthma
 Immediate hypersensitivity (type 1) response
 Most common chronic illness in children
 Tends to occur in children with atopy or hypersensitive to
allergens.
 pollens, molds, house dust, food, cold air, irritating
odors, air pollutants (e.g. cigarette smoke)
 Mast cells release histamine and leukotrines  triad of
inflammation, bronchoconstriction, and increased mucus
production  diffuse obstructive and restrictive airway
disease

Assessment
 History
 what the child was doing at the time of the attack
 what actions were taken by the parents or child to
decrease or arrest the symptoms
 describe the home environment, including any
pets, the child’s bedroom, outdoor play space,
classroom environment, and type of heating in
the house, etc.
 Physical Assessment
 wheezing so loud it can be heard without
auscultation
 Cyanosis
 Elevated eosinophil count
 Bronchospasm  CO2 trapping and retention 🡪
air-filled lungs  hyperresonant to percussion
 Longer expiration phase than inspiration
 Retractions
 Decreased wheezing means less air can go in 
hypoxemia  cyanosis
 Chronic sufferers:
 barrel-shaped chest
 clubbing of fingernails

Therapeutic Management
 Goals of therapy:
 avoidance of allergen by environmental control
 skin testing and hyposensitization to identified
allergens
 relief of symptoms by pharmacologic agents
 Cough suppressants are CONTRAINDICATED
 Pharmacological Tx:
  inhaled anti-inflammatory corticosteroid such as
fluticasone
 long-acting bronchodilator at bedtime
 short-acting beta-2–agonist bronchodilator, such
as albuterol or terbutaline
 leukotriene receptor antagonists such as
montelukast
 WOF dehydration
 Encourage to drink fluids, but avoid milk or milk
products

Status Asthmaticus
 Child fails to respond to first-line therapy (aerosol
administration of a bronchodilator)
 an extreme emergency

Assessment
 Acute respiratory distress
 Increased HR, RR
 O2 sat, PO2 low
 PCO2 elevated 🡪 acidosis
 Breath sounds limited (wheezing no longer heard)
 Often triggered by respiratory infection
 obtain cultures from coughed sputum
 broad-spectrum antibiotics until culture results
are available

Therapeutic Management
 Continuous nebulization with an inhaled beta-2-agonist
 IV corticosteroids
 Oxygen via face mask or nasal cannula to
 maintain the PO2 at more than 90 mm Hg.
 Drinking tends to aggravate coughing  IVF of D5
0.45NaCl
 Do not offer cold drinks  can trigger bronchospasm
 Monitor I&O, urine specific gravity

Pneumonia
 Infection and inflammation of the alveoli
 Types: hospital-acquired and community acquired
 May be bacterial, viral or aspiration
 Pneumocystis carinii pneumonia – associated with HIV/AIDS

Pneumococcal pneumonia
 Therapeutic Management
 Antibiotics: ampicillin or a third-generation
cephalosporin
  Amoxicillin-clavulanate (Augmentin) -
penicillin-resistant organisms
 Children need rest to prevent exhaustion
 Turn and reposition a child frequently to avoid pooling
of secretions
 IV therapy to supply necessary fluids; infants may tire
of sucking
 Humidified oxygen
 Assess oxygen saturation via pulse oximeter
 Chest physiotherapy
 Pneumococcal vaccine

Viral pneumonia
 generally caused by the viruses of upper respiratory tract
infection: the RSVs, myxoviruses, or adenoviruses.
 Assessment
 Si/sx of URTI for first 1-2 days 🡪 low-grade fever,
nonproductive cough, tachypnea
 Diminished breath sounds and fine rales upon
auscultation
 RSV may cause apnea
 CXR: diffuse infiltrated areas
 Therapeutic Management
 Symptomatic management
 Anti-pyretics
 IV fluid if w/ dehydration

Rheumatic Fever
 Autoimmune disease  reaction to group A beta-hemolytic
streptococcal infection
 Inflammation  fibrin deposits on the endocardium and
valves, esp. mitral valve, as well as major body joints.
 Often follows an attack of pharyngitis, tonsillitis, scarlet fever,
“strep throat”, or impetigo.
 Occurs most often in children 6-15 y/o, peak incidence at 8
y/o.
 Children do not develop immunity to streptococcal infections
 infections can recur
 Si/Sx of original infection subside in a few days, child appears
well  after 1-3 weeks, onset of rheumatic fever symptoms

Assessment
 Jones criteria
 Major
 Carditis
 Erythema marginatum – macular rash found
 predominantly
 on the trunk
 Subcutaneous nodules
 Sydenham’s chorea – sudden involuntary
movement of the
 limbs
 Polyarthritis
 Minor
 Arthralgia
 Fever
 Hx of previous rheumatic fever; prolonged
PR interval
 Elevated ESR, C-reactive protein,
leukocytosis

Therapeutic Management
 Full course is 6-8 weeks
 Maintain on bedrest during acute phase of illness
 Monitor VS, apical pulse
 Penicillin therapy; single IM benzathine penicillin
 Oral ibuprofen – arthralgia, inflammation
 Corticosteroids – if not responding to ibuprofen
 Phenobarbital, diazepam – chorea
 Digoxin, diuretics – if heart failure is present

Kawasaki Disease
 Mucocutaneous lymph node syndrome
 A febrile, multisystem disorder that occurs almost exclusively
in
 children before the age of puberty
 The peak incidence is in boys under 4 years of age
 Vasculitis (inflammation of blood vessels) is the principal (and
life- threatening) finding because it can lead to formation of
aneurysm and myocardial infarction
 Infection  altered immune function  increased antibody
production  circulating immune complexes (antigen-
antibody) bind to the vascular epithelium  inflammation of
blood vessels  aneurysm, platelet accumulation, thrombi
formation

Assessment
 Acute phase (Stage 1)
 High fever (39-40C) that doesn’t respond to
antipyretics
 Lethargic, or irritable
 Reddened swollen hands and feet
 Conjunctivitis
  Strawberry tongue and red, cracked lips
 Rashes
 Enlarged cervical lymph nodes
 Abdominal pain, anorexia, diarrhea
 Arthritic joints
 WBC, ESR elevated
 Subacute phase (10 days after onset)
 Desquamation, esp. on palms and soles
 PC rises
 Convalescent phase (stage II)
 25th-40th day
 Stage III
 From 40 days until ESR returns to normal

Treatment
 ASA, ibuprofen
 Abciximab is a platelet receptor inhibitor specific for
Kawasaki disease
 IV immune globulin (IVIG)
 Children should not receive routine
immunizations while taking IVIG or the
immunization will be ineffective.
 Steroids are contraindicated

DISORDERS OF THE GASTROINTESTINAL SYSTEM

Pyloric Stenosis
 Pyloric sphincter - opening between the lower portion of the
stomach and the beginning portion of the intestine, the
duodenum
 Narrowing in the pyloric sphincter, possibly due to
hypertrophy or hyperplasia of the muscles surrounding the
sphincter

Assessment
 At 4 to 6 weeks of age, infants begin to vomit almost
immediately after each feeding  projectile vomiting
 Formula-fed – at 4 weeks; breastfed – at 6 weeks onset
 Sour-smelling vomitus
 Disinterest in eating, excessive drooling, or chewing on
tongue suggests nausea
 History taking:
 What is the duration? Begins at 6 weeks of age
 What is the intensity? Projectile vomiting
 What is the frequency? Immediately after eating
 What is the description of the vomitus? Sour but
contains no bile
 Is the infant ill in any other way? No

NOTE: Fluid is unable to pass
easily through the stenosed
and hypertrophied pyloric
valve
 Signs of dehydration: lack of tears, dry mucous
membranes, sunken fontanelles, fever, decreased UO,
poor skin turgor, weight loss
 Alkalosis  hypopnea
 A definitive diagnosis is made by watching the infant
drink.
 Before the child drinks - attempt to palpate the
right upper quadrant of the abdomen for a pyloric
mass – round and firm approximately the size of
an olive
 As the infant drinks, observe for gastric peristaltic
waves passing from left to right across the
abdomen. The olive-size lump becomes more
prominent. The infant vomits with projectile
emesis
 UTZ  hypertrophied sphincter
 Endoscopy  direct visualization
Therapeutic Management
 Surgical or laparoscopic correction (pyloromyotomy)
 Correct electrolyte imbalance/dhn/starvation pre-op
 IVF PNSS or D5NSS
 NPO
 Pacifier for non-nutritive sucking

Intussusception
 Invagination of one portion of the intestine into another
 Usually occurs in the second half of the first year of life
 Infants <1 year old: idiopathic
 Infants >1 year old: “lead point”
 Meckel’s diverticulum, polyp, hypertrophy of Peyer’s
patches,
 bowel tumors
 The point of the invagination is generally at the juncture of
the distal ileum and proximal colon

Assessment
 During peristaltic wave: child will draw up legs and cry
(severe pain); may vomit
 Vomitus will begin to contain bile
 After approx. 12 hours, blood appears in stool and
possibly in vomitus
 “currant jelly” appearance
 If with necrosis: elevated temp, peritoneal irritation
(tender abdomen, guarding), increased WBC, rapid
pulse
 History taking
  What is the duration of the pain? It lasts a short
time, with
 intervals of no crying in between.
 What is the intensity? Severe
 What is the frequency? Approximately every 15 to
20 minutes
 What is the description? The child pulls up legs
with crying.
 Is the child ill in any other way? Yes. Vomits;
refuses food; states stomach feels “full.”
 Confirmed by ultrasound or CT scan

Therapeutic Management
 Surgical emergency
 Reduction of the intussusception must be done
promptly by either instillation of a water-soluble
solution, barium enema, or air (pneumatic insufflation)
into the bowel or surgery to reduce the invagination
before necrosis of the effected portion of the bowel
occurs
 Observe the child for 24 hours for recurrence of
intussusception

Necrotizing Enterocolitis (NEC)

 The bowel develops necrotic patches, interfering with
digestion and possibly leading to a paralytic ileus. Perforation
and peritonitis
 may follow
 Shock or hypoxia  vasoconstriction of blood vessels 
ischemia or poor perfusion  necrosis
 Lower incidence in breastfed compared to formula-fed

Assessment
 Distended abdomen; delayed gastric emptying 🡪 return
of undigested milk of more than 2mL
 (+) occult blood in stool
 Apneic episodes, si/sx of blood loss d/t intestinal
bleeding: dec. BP, ineffective thermoregulation
 X-ray: air invading intestinal wall

Therapeutic Management
 Put on NPO  IV, TPN
 Antibiotics
 Handle the abdomen gently to lessen the possibility of
bowel perforation
 Surgical removal of necrosis
 If perforation occurs  peritoneal drainage, laparotomy
  Temporary colostomy

Appendicitis
 Inflammation of the appendix
 The most common cause of abdominal surgery in children
 Fecal material enters the appendix 🡪 hardens and obstructs
the appendiceal lumen 🡪 inflammation, edema 🡪 compression
of blood vessels, cellular malnutrition 🡪 necrosis and pain
 If the condition is not discovered early enough, the necrotic
area will rupture and fecal material will spill into the
abdomen, causing peritonitis—a potentially fatal condition

Assessment
 Simple gastroenteritis
 Pain is a late symptom
 Diagnosis via symptom cluster: anorexia, pain,
tenderness in the
 RLQ, N/V, elevated temp, leukocytosis
 Abdominal pain is diffuse at first, then localized to RLQ
 (McBurney’s point)
 Rebound tenderness
 Reduced or absent bowel sounds
 Ultrasound, CT scan to confirm the appendicitis
 History Taking
 How was the child on Monday? Not herself. She
was not eating
 How was she Monday night? She had generalized
abdominal pain
 Tuesday morning? She had sharp localized pain
 Now? She has localized pain, vomiting, and fever

Therapeutic Management
 Surgical removal of the appendix prior to rupture
 Ruptured appendix:
 Position child in semi-Fowler’s
 IV for hydration
 Antibiotics
 Assess for signs of peritonitis: board-like abdomen,
shallow respirations, increased temp

Celiac Disease
 Malabsorption syndrome; gluten-induced enteropathy
 Sensitivity or abnormal immunologic response to protein,
particularly the gluten factor of protein found in grains—
wheat, rye, oats, and barley
 Ingestion of gluten 🡪 changes in intestinal mucosa or villi 🡪
prevents food absorption, esp. fat 🡪 steatorrhea, ADEK

OGTT  oral glucose
tolerances test
Biopsy  medical test that
involves extraction of sample
cells/tissue for examination to
determine presence of a
disease
Hirschsprung’s Disease
Ganglion  collection of
neuronal bodies found in the
voluntary and autonomic
branches of the peripheral
nervous system (PNS)
Chromosome 10  genes that
deficiency, distended abdomen
 Rickets, loss of calcium from bones, hypoprothrombinemia,
hypochromic anemia, hypoalbuminemia
 Occurs most frequently in children of a northern European
background
 increased incidence in children of type 1 diabetes mellitus, IgA
deficiency, and Down syndrome
Assessment
 Child tends to be anorectic and irritable; fall behind
other children their age in height and weight
 Appear skinny, with spindly extremities and wasted
buttocks
 Face may be plump and rounded
 History
 bulky stools, malnutrition, distended abdomen,
and anemia
 become noticeable between 6 and 18 months
 Serum analysis of antibodies against gluten (IgA
antigliadin antibodies)
 biopsy of the intestinal mucosa (done by endoscopy)
 OGTT
 Stool test for fat content
Therapeutic Management
 Gluten-free diet for life
 Water-soluble forms of vit. A & D; iron and folate
supplements
 Celiac Crisis
 Occur when child develops any type of infection
 Extreme symptoms
 Aganglionic megacolon
 Absence of ganglionic innervation to the muscle of a section
of the bowel, usually the lower portion of the sigmoid colon
just above the anus
 Absence of nerve cells 🡪 no peristaltic waves in the section 
chronic constipation, ribbonlike stool 🡪 bowel proximal to the
obstruction dilates 🡪 abdominal distention
 Gene abnormality on chromosome 10
 Higher incidence among siblings
 More often in males than in females
Assessment
 Infants who fail to pass meconium by 24 hours;
abdominal distention
provide instructions for  Symptoms may not become apparent until 6-12mos of
making protein age
 History of constipation:
 What is the duration of the constipation? It may
have been a problem from birth
 What do parents mean by constipation? Children
do not have a bowel movement more than once a
week
 What is the consistency of the stool? Ribbonlike
or watery
 Is the child ill in any other way? Children with
aganglionic disease of the intestine tend to be
thin and undernourished, sometimes deceptively
so because their abdomen is large and distended
 True constipation – examining finger will touch hard,
caked stool
 With Hirschsprung’s – rectum is empty
 Barium enema – use with caution
 Biopsy of affected segment – definite; will show the lack
of innervation
 Anorectal manometry - technique to test the strength or
innervation of the internal rectal sphincter by inserting a
balloon catheter into the rectum and measuring the
pressure exerted against it

Therapeutic Management
 Dissection and removal of the affected section, with
anastomosis of the intestine (termed a pull-through
operation)
 In infants, two-stage surgery:
 Temporary colostomy
 Bowel repair at 12-18 months

DISORDERS OF THE GENITOURINARY SYSTEM

Urinary Tract Infection (UTI)
 Occurs more often in females than in males
 Ascending infection from perineum most common, usually
gram- negative rods, such as E. Coli

Assessment
 Pain on urination, frequency, burning, and/or hematuria
 With cystitis: low grade fever, mild abdominal pain,
enuresis
 Pyelonephritis: high fever, abdominal or flank pain,
vomiting, malaise
 Any child with a fever and no demonstrable cause on
physical examination should be evaluated for UTI
  Urine c/s – clean catch, suprapubic aspiration,
catheterization
 Bacteriuria: bacterial colony count >100,000/mL
 Negative: <10,000
 Proteinuria – d/t presence of bacteria
 Hematuria – mucosal irritation
 Elevated pH >7

Therapeutic Management
 Oral antibiotics specific to causative organism
 IOFI – increase oral fluid intake
 Cranberry juice – acidifies urine 🡪 more resistant to
bacterial growth
 Mild analgesic e.g. Acetaminophen

Glomerulonephritis
 Inflammation of the glomeruli of the kidney.
 Usually occurs as an immune complex disease after infection
with nephritogenic streptococci (most commonly subtypes of
gABHS)
 Complement – a cascade of proteins activated by antigen-
antibody reactions and actually plufs or obstructs glomeruli
 Complement fixation reaction  tissue damage 
intravascular coagulation occurs in the minute renal vessels 
ischemic damage  scarring and decreased glomerular
function  decreased GFR (glomerular filtration rate) 
accumulation of Na and H2O in the bloodstream;
inflammation increases permeability  protein molecules
escape into the filtrate

Assessment
 History of recent respiratory infection (within 7-14 days)
or impetigo
 (within 3 weeks)
 Sudden onset hematuria and proteinuria – 24-hr urine
collection
 Urine appears tea-colored, reddish-brown, or smoky
 Oliguria
 Elevated urine specific gravity
 Abdominal pain, anorexia, vomiting
 Low-grade fever, headache
 Edema
 Hypertension d/t hypervolemia
 Cardiac involvement r/t difficulty managing excessive
plasma fluid
 Orthopnea
 Cardiac enlargement
  Enlarged liver
 Pulmonary edema
 Galloping heart rhythm
 ECG: T-wave inversion, prolonged PR interval
 Heart failure
 Hemodynamics:
 Hypoalbuminemia d/t massive proteinuria
 Low serum complement
 Mild anemia
 Increased ESR rate
 Increased urea, BUN, creatinine
 BP 160/100 and higher  encephalopathy  headache,
irritability, seizures, vomiting, coma or lethargy

Therapeutic Management
 Course of AGN: 1-2 weeks
 Little specific therapy
 Heart failure
 Place child in semi-Fowlers, digitalization, O2
therapy
 Diastolic pressure >90 mmHg: antihypertensive therapy
(Ca channel blocker)
 Phosphate binders, kayexalate

INFECTIOUS DISEASES
Rubella (German Measles)
 Causative Agent: Rubella virus
 Incubation period: 14-21 days
 Period of communicability: 7 days before to approx. 5 days
after rash appears
 Mode of transmission: Direct and indirect contact with
droplets
 Immunity: Contracting the disease offers lasting natural
immunity; a high rubella titer reveals infection has occurred
 Active artificial immunity: Attenuated live virus vaccine
 Passive artificial immunity: Immune serum globulin is
considered for pregnant women

Assessment
 1-5 days prodromal period
 Low-grade fever
 Headache
 Malaise
 Anorexia
 Mild conjunctivitis
 Sore throat, mild cough
 Swollen lymph nodes
  After prodromal period
 A discrete pink-red maculopapular rash begins on
the face, then spreads downward to the trunk and
extremities.
 On 3rd day, rash disappears
 (-) desquamation; if so, fine flaking of the skin

Management
 Comfort measures for rash
 Antipyretic, analgesic
 Droplet precaution for 7 days after onset

Measles (Rubeola)
 Causative agent: Measles virus
 Incubation period: 10 to 12 days
 Period of communicability: Fifth day of incubation period
through the first few days of rash
 Mode of transmission: Direct or indirect contact with droplets
 Immunity: Contracting the disease offers lasting natural
immunity
 Active artificial immunity: Attenuated live measles vaccine
Passive artificial immunity: Immune serum globulin

Assessment
 10- to 11-day prodromal period
 Lymphoid tissue becomes enlarged
 High fever (39.5-40C), malaise
 2nd day of prodromal period
 coryza – rhinitis and a sore throat
 Conjunctivitis with photophobia
 Cough
 Koplik’s spots – small, irregular, bright-red spots
with a blue-white center point on buccal
membrane
 4th day of fever
 Deep-red maculopapular eruption begins at the
hairline of the forehead, behind the ears, and at
the back of the neck and then spreads to the face,
the neck, upper extremities, trunk, and finally the
lower extremities
 After 5-6 days, rash completely fades  fine
desquamation

Management
 Comfort measures for rash
 Antipyretic, decongestants
 WOF complications: pneumonia, otitis media, airway
 obstruction, acute encephalitis

Chickenpox (Varicella)
 Causative agent: Varicella-zoster virus
 Incubation period: 10 to 21 days
 Period of communicability: 1 day before the rash to 5 to 6
days after its appearance, when all the vesicles have crusted
 Mode of transmission: Highly contagious; spread by direct or
indirect contact of saliva or vesicles
 Immunity: Contracting the disease offers lasting natural
immunity to chickenpox; may be reactivated at a later time as
herpes zoster (shingles)
 Active artificial immunity: Attenuated live virus vaccine
 Passive artificial immunity: There is little passive placental
immunity to chickenpox

Assessment
 Low-grade fever, malaise
 In 24hrs, rash that begins as macule 🡪 papule (6-8hrs)
 vesicle  crust
 Lesions are usually 2-3mm in diameter, accompanied by
elevated temp, mostly found in the trunk

Therapeutic Management
 Allow scabs to crust and fall of naturally; picking on
scabs will leave a white, round, slightly indented scar at
the site
 Advise children not to scratch and remove scabs
 Antihistamine, antipyretic
 Acyclovir
 Airborne and contact precaution until all lesions are
crusted
 Complications: secondary infection of lesions,
pneumonia, and encephalitis

Poliovirus Infections: Poliomyelitis

 Causative agent: Poliovirus
 Incubation period: 7 to 14 days
 Period of communicability: Greatest shortly before and after
onset of symptoms, when virus is present in the throat and
feces (1 to 6 weeks)
 Mode of transmission: Direct and indirect contact
Polio  Greek word for
 Immunity: Contracting the disease causes active immunity
“grey”, the color of the spinal
against the one strain of virus causing the illness.
cord after it atrophies from the
 Active artificial immunity: Inactivated polio virus vaccine (IPV)
effect of the poliomyelitis virus
 Passive artificial immunity: None
 Polio is Greek for “gray” – the color of the spinal cord after it
 atrophies from the effect of the poliomyelitis virus

Assessment
 Enters via GI, where it multiplies
 Fever, headache, nausea, vomiting, abdominal
pain
 Moderate pain of the neck, back, and legs soon
develops
 CSF – increased protein and lymphocytes
 Followed by intense pain and tremors of extremities 
paralysis occurring immediately or over a period of 1-7
days
 Kernig’s sign – test for meningeal irritation
 Tripod sign – cannot sit without placing both arms and
hands behind them to brace themselves
 DTR are hyperactive at first, then diminish as CNS is
fully invaded
 Laryngeal paralysis makes swallowing or talking difficult
 Respiratory paralysis can halt respiration

Therapeutic Management
 Bedrest
 Analgesia, moist hot packs
 Long-term ventilation
 Progressive muscle atrophy (survivors) or severe
arthritis in late
 adulthood

Mumps (Epidemic Parotitis)

 Causative agent: Mumps virus
 Incubation period: 14 to 21 days
 Period of communicability: Shortly before and after onset of
parotitis
 Mode of transmission: Direct or indirect contact
 Immunity: Contracting the disease gives lasting natural
immunity
 Active artificial immunity: Attenuated live mumps vaccine
Passive artificial immunity: Mumps immune globulin

Assessment
 Fever, headache, anorexia, malaise
 Within 24 hours, “earache” occurs, but child will point
to the jawline just in front of the ear lobe.
 Chewing movements aggravate the pain
 By next day, parotid gland is swollen and tender
 Boys also may develop testicular pain and swelling
 Therapeutic Management
 Soft or liquid die until swelling recedes (about 6 days)
 Analgesics, antipyretic
 Droplet and standard precautions
 Children are infectious for at least 5 days after
symptoms appear
 Complications: mumps orchitis, meningoencephalitis,
severe permanent hearing impairment

Diphtheria
 Causative agent: Corynebacterium diphtheriae (Klebs- Löffler
bacillus)
 Incubation period: 2 to 6 days
 Period of communicability: Rarely more than 2 weeks to 4
weeks in untreated persons; 1 to 2 days in children treated
with antibiotics
 Mode of transmission: Direct or indirect contact
Diphtherial Bacilli invade and  Immunity: Contracting the disease gives lasting natural
grow in nasopharynx  immunity
exotonin production   Active artificial immunity: Diphtheria toxin given as part of
massive cell necrosis and DTaP vaccine
inflammation  necrosing  Passive artificial immunity: Diphtheria antitoxin
material feeds the bacilli more  Diphtheria bacilli invade and grow in nasopharynx  exotoxin
production  massive cell necrosis and inflammation 
necrosing material feeds the bacilli more

Assessment
 Characteristic gray membrane on the nasopharynx
 Purulent nasal discharge
 Brassy cough
 If untreated, myocarditis, CNS involvement may occur
 Diagnosis via throat culture

Therapeutic Management
 IV antitoxin
 Penicillin or erythromycin
 Complete bedrest
 Droplet precaution
 WOF airway obstruction  ET intubation

Whooping Cough (Pertussis)

 Causative agent: Bordetella pertussis
 Incubation period: 5 to 21 days
 Mode of transmission: Direct or indirect contact
 Period of communicability: Greatest in catarrhal (respiratory
illness) stage
 Immunity: Contracting the disease offers lasting natural
 immunity
 Active artificial immunity: Pertussis vaccine given as part of
DTaP vaccine
 Passive artificial immunity: Pertussis immune serum globulin

3 Stages
1. Catarrhal stage
 URTI symptoms, coryza, sneezing, lacrimation,
cough, low grade fever
 Children are irritable and listless
 Lasts from 1-2 weeks
2. Paroxysmal stage
 Lasts 4-6 weeks
 Cough changes from mild to paroxysmal, 5-10
short, rapid coughs followed by a “whoop” or
high-pitched crowing sounds
3. Convalescent stage
 Gradual cessation of coughing and vomiting
 Children younger than 6 months of age: “whoop”
of the cough may be absent
 B. pertussis may be cultured from nasopharyngeal
secretions
 Increased WBC

Therapeutic Management
 Maintain on bedrest, seclude from environmental
factors
 Frequent small meals
 May be admitted to health care facility d/t tenacious
secretions needing airway suction
 Full 10-day course erythromycin/azithromycin
 Droplet precaution until 5 days after child starts
antibiotics
 Complications: pneumonia, atelectasis, emphysema,
seizures from asphyxia, epistaxis, alkalosis and
dehydration if with insufficient fluid intake

Helminthic Infections
 Helminths are pathogenic or parasitic worms
 Because children tend to be careless about washing their
hands before eating or tend to suck their thumbs, they are
prone to these infections

Roundworms (ascariasis)
 Eggs are excreted in feces  larvae hatch and
penetrate intestinal wall and enter circulation
 Loss of appetite, nausea, vomiting
  Intestinal obstruction may occur
 Anthelmintic – pyrantel pamoate

Pinworms
 Small, white, threadlike worms live in the cecum
 At night, female pinworm travels to anus to deposit
eggs on the anal and perianal region  child awakens
at night crying and scratching
 Some eggs are carried from child’s fingernails to the
mouth, cycle is repeated
 Worms are large enough to be seen if child’s buttocks
are separated while sleeping.
 Press a piece of cellophane tape against anus 
microscopic examination to reveal pinworm eggs
 Treatment: single dose mebendazole or pyrantel
pamoate
 All family members are treated for pinworm infestation
 Teach child to avoid nail biting and to wash their hands
before food preparation or eating

SUMMARY