Criteria for Respiratory Distress in Children With Pneumonia

Signs of Respiratory Distress

1. Tachypnea, respiratory rate, breaths/mina
    Age 0–2 months: >60
    Age 2–12 months: >50
    Age 1–5 Years: >40
    Age >5 Years: >20
2. Dyspnea
3. Retractions (suprasternal, intercostals, or subcostal)
4. Grunting
5. Nasal flaring
6. Apnea
7. Altered mental status
8. Pulse oximetry measurement <90% on room air

Variables PCAP – A PCAP – B PCAP – C PCAP – D

Minimal Risk Low Risk Moderate Risk High Risk
Co – morbid illness None Present Present Present
Compliant caregiver Yes Yes No No
Ability to F/U Possible Possible Not possible Not possible
(+)Dehydration None Mild Moderate Severe
Ability to feed Able Able Unable Unable
Age >11 months >11 months <11 months <11 months
Respiratory Rate
2 - 12 months >50/min >50/min >60/min >60/min
1 – 5 years >40/min >40/min >50/min >50/min
>5 years >30/min >30/min >35/min >35/min
Signs of respiratory failure Supraclavicular/intercostal
a. Retraction None None Intercostal/subcostal /subcostal
b. Head bobbing Present Present
c. Cyanosis Present Present
d. Head grunting None Present
Signs of respiratory failure
a. Apnea None None None Present
b. Sensorium Awake Awake Irritable Lethargic, stupurous/comatose
Complications None None Present Present
Action plan OPD OPD Admit to regular ward Admit to ICU

Simple febrile seizures
Self – limiting
Short duration (<15 minutes)
Tonic – clonic features
No reoccurrence within the next 24
hours
No post – ictal pathology
Complex febrile seizures Newborn Screening in the Philippines
Longer duration (>15 minutes) Congenital hypothyroidism
May present as series of seizures with limited time Congenital adrenal hyperplasia
interval Galactosemia
New events may reoccur within the next 24 hours Phenylketonuria
Focal seizures, with several possible features: G6PD deficiency
 Clonic and/or tonic movements
 Loss of muscle tone
 Beginning on one side of the body, with
or without secondary generalization
 Head and/or eye deviation to one side
 Seizure activity followed by transient
unilateral paralysis (lasting minutes to
hours, occasionally days)
 Typhoid Fever NTS Gastroenteritis Nephrotic Nephritic
Etiology S. Typhi Nontyphoidal Salmonella
serovars (eg, S. Massive proteinuria Hematuria
typhimurium, S. enteritidis) Hypoalbuminemia Oliguria
Distribution of bacteria in Systemic infection Infection remains localized Edema Azotemia
immunocompetent host to intestine and mesenteric Hyperlipidemia/hyperlipiduria hypertension
lymph nodes
Incubation period 14 days <1 day
Common symptoms Fever, relative Diarrhea, abdominal pain,
bradycardia fever, headache, muscle
pains
Duration of symptoms 3 weeks <10 days
Predominant cell type in Mononuclear cells and Neutrophils
intestinal infiltrates lymphocytes
Fecal leukocytes Mononuclear cells Neutrophils

Overview
Self – limited disease in
infants occurring within
the first few hours of
life. Usually a result of
delayed clearance of
fetal lung liquid.
Can be acquired 1 of 3
ways: congenital,
during birth, or after
birth. Congenital
causes include
Toxoplasmoa gondii,
rubella, HSV, mumps,
adenoviruses, Listeria
monocytogenes, and
Mycobacterium
tuberculosis.
Group B strep are
responsible for most
cases acquired at
delivery.
Chlamydia trachomatis
is acquired during
passage through an
infected birth canal,
though it can also occur
after prolonged
membrane rupture.
Overview
Most common GI
medical/surgical
emergency occurring in
neonates. Multifactorial
etiology.
Characterized by variable
damage to the intestinal
tract.
Most commonly affects
the terminal ileum and
ascending colon.
Infants with compromised
placental blood flow are
prone to NEC. Also prone
are preemies.
IA
Mild non-specific Same as Stage
systemic signs such IA, with
as apnea, addition of
bradycardia, and grossly bloody
temperature stool.
instability.
Mild intestinal signs
such as increased
gastric residuals
and mild abdominal
distention
X-ray findings may
be normal or are
mild nonspecific
findings.
IA
NPO diet with antibiotics for 3 days. IVF
is provided, including TPN.
Note: antibiotic theraphy is usually ampicillin, aminoglycosided or 3 generation cephalosporin, and clindamycin or metronidazole.
TRANSIENT TACHYPNEA OF THE NEWBORN
Presentation Differential Diagnosis Workup Treatment Medication
Tachypnea with Congenital pneumonia ABG Supportive: Minimal medication.
variable grunting, Meconium aspiration Pulse Ox IVF and Antibiotics (Ampicillin
flaring, and retracting. syndrome CXR lavage or Gentamicin) may
Maternal history of Neonatal sepsis feedings. be used for 48 hours
caesarean delivery Pneumomediastinum Rarely an after birth until
without labor or Pneumothorax infant sepsis is ruled out.
precipitous delivery. Persistent newborn develops a
Resolution usually pulmonary hypertension picture of
occurs 72 hours after Respiratory distress worsening
birth. syndrome respiratory
distress.
NEONATAL PNEUMONIA
Sudden onset of Foreign body aspiration, ABG Empiric Outpatient: Not
fever, cough, and heart failure, malignancy, Pulse Ox antibiotic recommended for first 3
months of age. 1st line
tachypnea. Clinical atelectasis, pulmonary CXR treatment x drug is Amoxicillin. If
exam findings include embolus, pulmonary Blood 10 – 14 days. penicillin allergic,
tachypnea, rales, and hemorrhage, and cultures in Patient may clindamycin, levofloxacin,
retractions. sarcoidosis. Collagen hospitalize be switched to 3rd gen cephalosporins,
Abdominal pain is vascular disease. d patients. PO at time of or macrolides
common with basilar Environmental irritants, CBC with discharge. Inpatient: Neonate 1st
pneumonia. Atypical congenital lung anomalies. diff line is Ampicillin +
pneumonia may aminoglycoside. 1 month
present with dry, and up Ampicillin.
nonproductive cough,
For moderately or
headache, malaise, severely ill patients,
fever, and cefotaxime, ceftriaxone,
pharyngitis. and levofloxacin provided
broader coverage against
PCN$ pneumococci.
Azithromycin,
clarithromycin, or
levofloxacin should be
added to cover atypical
pathogens. Vanco for
MRSA.
NECROTIZING ENTEROCOLITIS
Presentation Differential Diagnosis Workup
Presentation: nonspecific findings such Hypoplastic left heart syndrome ABG
as vomiting, diarrhea, feeding Intestinal malrotation Abdominal
intolerance and high gastric residuals. Intestinal volvulus radiograph
Also may have abdominal distention Bacterial meningitis Abdominal US
and blood in stools. Neonatal sepsis Upper GI series
Omphalitis Paracentesis
PE: ↑abdominal girth, visible intestinal Prematurity
loops, obvious abdominal distention, Urinary tract infection
↓bowel sounds, change in stool Volvulus
pattern, hematochezia, erythema of GERD
abdominal wall, palpable abdominal Hirschsprung’s
mass. Systemic signs include Bacteremia
respiratory failure, ↓peripheral Coarctation of the aorta
perfusion, circulatory collapse.
Staging of NEC and Treatment
IB IIA IIB IIIA IIIB
Patient is mildly ill. Patient is moderately Patient has severe NEC Severely ill infant
ill. with an intact bowel. with perforated
Mild systemic signs bowel observed
as in IA. Stage I symptoms plus Dx requires all of the on X-ray in
Intestinal signs systemic signs of above conditions with addition to
include all signs moderate illness, such addition of hypotension, findings for IIIA.
present in stage I, as mild metabolic bradycardia, respiratory
with the addition of acidosis and mild failure, severe
absent bowel thrombocytopenia. metabolic acidosis,
sounds and coagulopathy, and/or
abdominal Abdominal neutropenia.
tenderness examination reveals
definite tenderness, Abdominal examination:
perhaps some marked distention with
erythema or other signs of generalized
discoloration, and/or peritonitis.
RLQ mass.
X-ray: definitive
X-ray show portal evidence of ascites.
venous gas w/ or w/out
ascites.
Treatment by Stage
IB IIA IIB IIIA IIIB
Support for respiratory and cardiovascular NPO x 14 days, fluid Surgical
failure, including fluid resuscitation, NPO, and resuscitation, inotropic intervention.
antibiotics x 14 days. support, and ventilator
support.
Surgical consultation should be considered.
Surgical consultation
After stabilization, TPN should be provided should be obtained.
during the period that the infant is NPO.
TPN should be
provided during NPO
period.
rd
 NEPHROTIC SYNDROME
Overview Presentation Differential Workup Treatment Medication
Diagnosis
Characterized by First sign is Diabetic nephropathy U/A Pediatrics: Corticosteroids,
proteinuria, swelling of the Focal segmental Urine sediment Diuretics cyclophosphamide,
hypoalbuminemia, and face, followed glomerulosclerosis examination (Furosemide or and cyclosporine
edema. by swelling of Chronic Urinary protein spironolactone) are used to induce
the body. glomerulonephritis measurement remission.
Nephrotic range Foamy urine Membranous Renal biopsy for: Adult:
proteinuria > 3 gm/day. may be present. glomerulonephritis Congenital nephrotic Diuretics Diuretics to reduce
Hematuria and HIV nephropathy syndrome Anticoagulation edema.
Many specific causes hypertension IgA nephropathy Children >8 y at Hypolipidemic
including minimal change may be present. Light chain onset agents ACE inhibitors to
nephropathy, focal associated renal Steroid resistance If 2ndary to DM, reduce proteinuria.
glomerulosclerosis, disorders Frequent relapses or ACE inhibitors
membranous Minimal change steroid dependency Rituximab has
nephropathy, and disease Significant nephritic been effective in
hereditary nephropathy. Nephritis, radiation manifestations cases relapsing
Sickle cell Serum albumin after prednisone
There is usually damage nephropathy Serologic tests treatment.
to the glomerular (ANCA, ANA, Hep B
structure, such as the or C, HIV, anti-
endothelial surface, dsDNA, ASO)
glomerular basement
membrane, or the
podocytes.

ACUTE GLOMERULONEPHRITIS
Overview Presentation PE Differential Workup Medication
Diagnosis
Sudden onset of Symptoms:  Periorbital and/or Anaphylactoid CBC Antibiotics for
hematuria,  Hematuria pedal edema purpura with Electrolytes underlying
proteinuria, and RBC  Oliguria  Edema and HTN due nephritis BUN/Creatinine infection.
casts. Clinical  Edema (peripheral or to fluid overload Chronic GN Complement Loop diuretics
picture is often periorbital)  Crackles with an acute levels for edema
accompanied by  Headache  Elevated JVP exacerbation U/A and HTN.
hypertension, edema,  Shortness of breath or  Ascites and pleural Idiopathic 24 hr urine Vasodilator
azotemia (↓GFR), dyspnea on exertion effusion (possible) hematuria study for severe
and renal salt and  Possible flank pain Maybe: Familial Streptozyme/AS HTN and
water retention. Most  Rash nephritis O titer encephalopat
common etiology is Symptoms of systemic dz  Pallor IgA nephritis Nephritis- hy.
following that can ppt AGN: MPGN associated
 Renal angle fullness
streptococcal  Triad of sinusitis, Lupus nephritis protease
or tenderness, joint
infection (PSGN). pulmonary infiltrates, GN of chronic (NAPR) TREATMENT
swelling, or
and nephritis infection elevated in pts :
tenderness
Most often, patient is (suggesting Wegener’s VasculitiS with Mainly
 Hematuria
a boy, 2-14 years, granulomatosis) streptococcal supportive.
who suddenly  Abnormal neurologic infxn with GN Sodium and
 Nausea and vomiting, examination or altered
develops puffiness of US to evaluate fluid
abdominal pain, and LOC
the eyelids and facial kidney size. <9 restriction.
purpura (Henoch-  Arthritis
edema in the setting cm suggests Bed rest until
Schonlein purpura) Other signs:
of a extensive signs of
 Arthralgias (SLE)  Pharyngitis
poststreptococcal scarring and glomerular
infection. Urine is  Hemoptysis  Impetigo low likelihood of inflammation
dark and scanty. BP (Goodpasture’s or  Respiratory infection reversibility. and
may be elevated. idiopathic progressive  Pulmonary circulatory
Nonspecific infection glomerulonephritis) hemorrhage congestion
include weakness,  Skin rashes  Heart murmur subside.
fever, abdominal (Hypersensitivity  Scarlet fever
pain, and malaise. vasculitis, SLE, HSP,  Weight gain
There is a latent or cryoglobulinemia)
 Abdominal pain
period of 3 weeks  Anorexia
following strep  Back pain
infection.  Oral ulcers

PHYSIOLOGIC CHANGES IN THE NEWBORN

Respiratory
 Surfactant production increases at 24 weeks AOG
 Fluid compressed from lung during vaginal delivery.
 1st breath initiated by response to arousal to sound, temperature change, and touch. Chemical receptors further increase respiratory drive
in response to hypoxia and hypercarbia.
 1st breath overcomes airway resistance, inertia of fluid in airways, and surface tension of the air/fluid interface in the alveolus.
 Alveolar distension, cortisol, and epinephrine all stimulate type II pneumocytes to produce surfactant and reduce alveolar surface tension,
thereby facilitating lung expansion.
Cardiac
 Umbilical vessels constrict in response to stretching and increased oxygen content at delivery.
 Low resistance placenta is removed and systemic resistance increases.
 Circulation through ductus venosus is reduced causing passive closure over the following 3-7 days and reducing blood return to IVC.
 Lung expansion drops pulmonary vascular resistance, increasing resistance to left atrium.
 Increased pressure to left atrium and decreased pressure to right atrium functionally closes the foramen ovale within the first few breaths of
life.
 Physiological reverse shunt from left to right commonly occurs.
 Resultant drop in pulmonary artery pressure and increase in SVR reverses flow across ductus arteriosus from left to right.
 Ductus arteriosus is affected by blood oxygen content and circulating prostaglandins. The potent dilator PGE2 produced by placenta is lost
at birth facilitating DA closure.
 Catecholamine surge at birth leads to improved myocardial function and increased CO.
Hematologic
 HbF is replaced by HbA
 Vitamin K dependent cofactors are low at birth. Therefore, all newborns are given vitamin K at birth.
Thermoregulation
 Heat produced by limb movement and brown fat.
Hepatic
 Conjugation of bilirubin not mature until 2 weeks after delivery. Unconjugated bilirubin levels rise within first 48 hours due to rapid
breakdown of HbF and immature liver.
Renal
 Glomeruli and nephrons are immature at birth.
 Renal immaturity also affects vitamin D formation and calcium homeostasis.
Nervous System
 Blood brain barrier will not mature until 6 months of age.
 Parasympathetic system predominates in neonates. So it is better developed to protect against hypertension than hypotension.