Peds respiratory disorders Flashcards

(54 cards)

1
Q

Neonatal Respiratory Distress Syndrome (RSD)

general

A

Also known as hyaline membrane disease
Condition caused by structural and functional immaturity of the lungs
Undeveloped parenchyma
Inadequate production of pulmonary surfactant (Type II pneumocytes)
Most common cause of respiratory distress in preterm infants
Frequent cause of morbidity and mortality in neonates

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2
Q

Neonatal Respiratory Distress Syndrome (RSD)

Epidemiology

A

Risk is inversely related togestational ageat delivery
Highestincidencein babies born < 28 weeks of gestation
Higherincidencein white male infants

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3
Q

RSD

etiology(3)

prematurity and surfactant

A

Conditions that cause fetalacidosis (may ↓surfactantsynthesisand/or activity)
Genetic mutations affecting production of surfactant proteins

Prematurity
Lack of mature type II alveolar cells → insufficientsurfactantproduction
Different lipid and protein composition ofsurfactantin an immature lung → less activesurfactant

Surfactantinactivation
Meconiumor blood inalveoli(more common in term infants)
Oxidative and mechanical stress such as from mechanicalventilation

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4
Q

RSD

maternal and C section

A

Maternal diabetes
Maternal hyperglycemia→ fetalhyperinsulinemia
↑Insulinantagonizes the action ofcortisol, delaying lungsurfactantproduction

Cesarean delivery(CD) without labor
In the absence of labor,cortisolproduction (as well as other hormonal factors) is decreased
Altered fluid clearance from the fetal lung compared with vaginal delivery

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5
Q

Normal Fetal Lungs
Surfactant surge

A

Fetallungs
Not functional forgas exchange, and are filled with fluid (amniotic fluid)
Theplacentaserves as the fetus’s respiratory organ

Surfactant
Lipid-dense secretion (~80% phospholipids)
Produced in fetal development to prepare for air-breathing at birth
Appears in amniotic fluid between 28-32 weeks gestation
Surge in surfactant levels after 36 weeks
Reducessurface tensionwithin thealveoli
Prevents alveolar collapse at the end of theexpiration
↓ Risk ofatelectasisand ventilatory-perfusion (V/Q) mismatch in thealveoli

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6
Q
A
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7
Q

Respiration at Birth and RDS

A
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8
Q

Premature Lungs

A

Surfactant deficiency causing ↑ surface tension

↑ pressure is required for alveolar expansion

Lung instability at end-expiration
Low lung volume and ↓compliance
Collapse of portions of thelungs(atelectasis) → V/Q mismatch

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9
Q

RDS

Clin man

S/Sx and on auscultation

A

Respiratory distress
Starts within minutes or hours after birth
Becomes progressively worse over the first 48–72 hours of life
Tachypnea
Nasal flaring
Retractions
Expiratorygrunting
Cyanosis(from right-to-left shunting)

On auscultation:
Breath sounds may be normal or diminished, with a harsh tubularquality
Bilateral fine basal crackles

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10
Q

RDS

Cxray

A

ChestX-ray
Low lung volume
Bilateral, diffuse ground-glass appearance
Air bronchograms
Gas-filled bronchi surrounded by alveoli filled with fluid
Arterial blood gas(ABG)
Hypoxemia – improves with O2
Hypercapnia as disease progresses
Respiratoryacidosis

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11
Q

RDS

Management pre delivery

A

Prevention
Most effective preventive method is to avoid preterm delivery, when possible

Determine fetal lung maturity by amniocentesis
Usually performed after 32 weeks
Assess surfactant levels
Lecithin-to-sphingomyelin (L/S) ratio
Presence or absence of phosphatidylglycerol

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12
Q

RDS

management for preterm delivery and post delivery

A

If an early delivery cannot be avoided, treatment includes:

Antenatal corticosteroid therapy
Enhancessurfactantsynthesisandrelease
Accelerates lung maturity
Indicated for preterm delivery
Steroids are given 24-48 hours before delivery

Exogenoussurfactantreplacement therapy
Beneficial to preterm infants born < 30 weeks gestation
Provides support until endogenous production begins
Administration within 30–60 minutes of life provides the most benefit
Administered via endotracheal or less-invasive route (nebulization)

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13
Q

RDS

resusitation

A

Resuscitation
Airway, breathing, andcirculation (ABCs)
Respiratory support especially for babies under 28 weeksgestational age
The goal is for effectiveventilationand oxygenation in the least invasive manner possible
Nasal continuous positiveairwaypressure (nCPAP)
Endotrachealintubationand assisted mechanicalventilation for respiratory failure
Extracorporeal membrane oxygenation (ECMO)
Treatment that uses a pump to circulate blood through an artificial lung back into the bloodstream

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14
Q
A
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15
Q

Kussmaul breathing

A

increased depth of ventilation, but the rate is rapid (diabetic ketoacidosis)

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16
Q
A
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17
Q

Croup

general

A

Also known as laryngotracheobronchitis
Characterized by severe inflammation of the upper airway and most commonly caused by a viral infection
Primarily affects children aged 6–36 months
Potential affected age range: 6 months to 15 years
More prevalent in the fall and early winter

Transmission:
Aerosol droplets released by sneezing and coughing or by contact with infected secretions

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18
Q

Croup

Etiology

A

Etiology
Viral (75% of cases)
Most common: parainfluenza virus types 1 and 2
Second most common: respiratory syncytial virus (RSV)
Other causes: adenovirus, coronavirus, measles, influenza virus, rhinovirus, enterovirus, herpes simplex virus, metapneumovirus
Bacterial: usually present with high fever, look sicker than viral

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19
Q

Croup

Patho

A

Virus/bacteria infects the nasal and pharyngeal mucosal epithelium through aerosol droplets
Infection spreads to the larynx and trachea via respiratory epithelium
Infection triggers the infiltration of white blood cells
Edema ensues inside the trachea, larynx, and large bronchi
Edema partially obstructs the airway

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20
Q

Croup

S/Sx

A

Nasal discharge
Congestion
Coryza
Spasmodic, barking cough (common at night)
Inspiratory stridor
– worsens with agitation
Fever
Hoarseness
Hoover’s sign (inward movement of the lower rib cage during inspiration)

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21
Q

Croup

Typical course (viral croup)

A

Initial symptoms:coryza, nasal congestion
12–48 hours:fever, barking cough, hoarseness,stridor
As disease progresses, respiratory distress (noted bytachypnea,dyspneaat rest, thoracic retractions, mental status changes) can occur
Disease lasts around 3–7 days (self-limited)

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22
Q

Croup

Dx

A

Clinical based on the presence of a“seal-like” barking cough and inspiratory stridor

for severe pts
Imaging
AP and lateral neck x-ray
Rule out other causes
Assess the severity of croup
AP neck x-ray usually shows a “steeple sign” which represents subglottic narrowing

Pearls & Pitfalls
Epiglottitis, retropharyngeal abscess, and bacterial tracheitis cause a more toxic appearance than croup and are not associated with a barking cough

24
Q

Croup

Westley Croup Score

A

Designed to measure severity of croup
Can be useful in determining treatment efficacy and patient disposition
Assesses 5 factors
Scores range: 0-17 points

25
# Croup Tx
Antipyretics **Corticosteroids** (high-dose dexamethasone) **Improvement in airway inflammation/**symptoms in 6–8 hours 0.6 mg/kg IM, IV, or orally once **Racemic epinephrine** given by nebulization (moderate and severe disease) 5 to 10 mg in 3 mL of saline every 2 hours Observe 3–4 hours after initial treatment Supplemental oxygen Cough medicines with dextromethorphan or guaifenesin should be avoided Antibiotics are only prescribed in cases of primary or secondary bacterial infection
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# croup Requirements for Outpatient Management
Non-toxic appearance 3-4 hours since the last nebulized racemic epinephrine Able to tolerate fluids **No stridor at rest** Normal pulse oximetry Reliable parents with a good understanding of return precautions Close follow-up for moderate or severe cases
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# Croup prognosis
Self-limiting disease that usually resolves within 3-7 days (80% of cases) Life-threatening illness, but rarely progresses to death Mortality occurs in <1% of intubated patients Out-of-hospital cardiac arrest may occur
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# croup complications
Complications (uncommon) Pneumonia Secondary bacterial tracheitis (high fever, toxic appearance, mucopurulent exudates in the trachea) Respiratory failure Pneumothorax Recurrent symptoms (5% of cases)
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# Acute bronchiolitis general
Acute inflammation of the small airways (bronchioles) most often secondary to viral infections Common cause of hospitalization in infants in the United States Peak incidence between **2-6 months of age** Seasonal preference: fall and winter 
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# Acute bronchiolitis Etiology
Viral infection: **Respiratory syncytial virus (RSV)** – 1/3 of cases Rhinovirus Less common: Human metapneumovirus, Parainfluenza virus, Influenza virus, Adenovirus, Mycoplasma pneumoniae , Pertussis
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# acute bronchilitis RF
Prematurity (born < 34 weeks) < 12 weeks of age Low birth weight (< 2.5 kg) Immunodeficiency Congenital heart disease Cystic fibrosis Not breastfed secondhand smoke
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# acute bronchilitis patho
Pathological changes occur within 24 hours of contact with a pathogen: Virus enters epithelial cells of terminal bronchioles Inoculation causes inflammation → **edema, mucus secretion, and epithelium sloughing** Sloughing and edema → **narrowing and obstruction of small airways** Narrowing results in atelectasis and symptoms appear Alveoli can over-inflate and become trapped with air ## Footnote look for kid with lots of secretion, runny nose like faucet
34
# acute bronciolitis Sx
Symptoms vary based on the severity of the disease: Initial 1–3 days (upper respiratory tract symptoms): Cough Congestion Rhinorrhea Peaks on day 3–5 (lower respiratory tract symptoms): **Wheezing and diffuse crackles** on lung exam Fever Shortness of breath
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# acute bronchiolitis Sx severe cases
Severe cases: Apnea in infants, especially during sleep Tachypnea Cyanosis Nasal flaring Grunting Intercostal retraction Hypoxia < 92% saturation
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# acute bronchiolitis Dx
Based on clinical suspicion:  Characteristic lower respiratory tract symptoms **Patients < 2 years** Presenting during the fall and winter seasons Routine testing is discouraged → no therapeutic value **Further investigation**:  Indications: high fever, severe presentation, history of comorbidities Evaluate comorbid conditions or superimposed infection: Complete blood count (CBC): leukocytosis  CXR: hyperinflation with atelectasis  RSV testing
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# acute bronchiolitis Tx mild/moderate cases
Mild-to-moderate cases Upright positioning during sleeping and feeds Use of cool-mist humidifier and antipyretic Bulb suctioning of oral and nasal secretions Maintain hydration and feeding Follow-up if patient worsens
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# acute bronchiolitis Severe tx
Severe (< 28 days old, apnea, lethargic) Hospital admission Humidified oxygen and nebulized hypertonic saline Suctioning of secretions IV hydration No evidence to support use of albuterol, epinephrine, or corticosteroids Complications - pneumonia and respiratory failure
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# RSV general
RNA virus; paramyxovirus family Transmission via droplets (coughing, sneezing, kissing, touching infected objects then touching mucus membranes) Seasonal epidemiology RSV seasonality was altered following the COVID-19 pandemic; it is unknown if or when RSV will return to normal seasonality
40
# RSV presentation
Presentation: Usually mild, cold-like symptoms Serious illness (infants and older adults) Highest risk among: Premature infants Young children with **congenital heart** or **chronic lung disease** Young children who are **immunocompromised** Adults 65 and older with compromised immune systems Adults 65 and older with underlying heart or lung disease
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Diseases Caused by Respiratory Syncytial Virus (RSV)
Infants: Acute bronchiolitis Pneumonia Acute otitis media Respiratory failure Immunocompromised or elderly adults:  Pneumonia Acute exacerbation of underlying chronic illness (COPD, asthma, congestive heart failure)
42
# RSV Dx
**Rapid antigen tests Most common test** Nasal washings or nasal swabs Results available in ~30 minutes RSV RT-PCR Molecular test that detects the genetic material of the virus More sensitive than antigen testing or viral culture Viral culture Declining use Costly and more difficult to perform Several days to obtain a results ## Footnote not normally done, does not change tx
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# RSV Tx Prophylaxis
Self-limited Supportive care Passive prophylaxis- for high risk kids **Palivizumab** Indicated for high-risk infant First dose just before the onset of RSV season Subsequent doses given at 1-month intervals (total of 5 doses)
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# whooping cough general What age is affected
Potentially life-threatening highly contagious bacterial infection of the respiratory tract caused by  Bordetella pertussis (gram-negative coccobacillus) Endemic worldwide Incidence in the United States is affected by: Immunity waning in previously vaccinated adolescents and adults Anti-vaccination movement Common and most severe in infants **< 1 year of age** Transmission Airborne droplets (coughing, sneezing, or speaking) or direct contact with oral or nasal secretions of an infected individual Often affects 100% of non-immune household contacts
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# whooping RF
Individuals at risk for contracting pertussis and/or severe disease include: Unvaccinated individuals Infants (especially < 4 months) Pregnant women Patients with an immunodeficiency Patients with an underlying respiratory condition (COPD) Older adults (> 65 years of age) Those caring for infants
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# whooping patho
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# whooping Catarrhal
Catarrhal – most infectious stage Lasts 1–2 weeks Presents with nonspecific symptoms of an upper respiratory tract infection: Low-grade fevers Coryza Sneezing Conjunctival injection
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# whoopin proxysmal
Paroxysmal Lasts 2–8 weeks  Presents with the characteristic intense coughing (≥5 rapidly consecutive forceful coughs) followed by an inspiratory “whooping” sound Frequently occurs at night Whooping occurs ,ore frequently in older children and toddlers Infants (< 6 months of age) may present with periods of choking or apnea (inability of the respiratory muscles to produce strong coughing) Viscid (sticky) mucus from the nares Post-tussive vomiting, shortness of breath (dyspnea), and cyanosis
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# whooping convalescent
Convalescent Lasts **4 weeks on average**, but may extend for months Characterized by the progressive reduction of all symptoms
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# whooping Dx and prevention
Strong suspicion from a complete history and physical examination Possible contact with other “whooping cough” cases Vaccination status **Vaccine does not provide full protection; pertussis needs to be considered even in vaccinated children!** **Laboratory confirmation is required Nasopharyngeal swab → culture (gold standard) or PCR testing** Only reliable during the first 2-3 weeks of the infection Serology testing Can be used up to several weeks (2-8 weeks) after the onset of symptoms A 2-fold rise in the antibody titer against pertussis is diagnostic
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# whooping Tx Hospitalization
Supportive care Suction to remove mucus from the throat Azithro Hospitalization with respiratory isolation: Infants < 1 Hypoxia Apnea Respiratory distress **Superimposed pneumonia** Unable to hydrate orally Oxygen administration may be required in severe cases
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# whooping Drug Tx
Macrolide Catarrhal stage → ameliorate the disease Paroxysmal stage → reduce the spread of pertussis, but do not affect the clinical course Azithromycin 10 mg/kg PO once daily x 5 days First-line choice for infants < 1 month of age Erythromycin 10 mg/kg PO every 6 hours x 14 days (maximum 2 g/day) Clarithromycin 7.5 mg/kg PO twice daily x 7 days (maximum 1 g/day) Macrolide allergy → trimethoprim-sulfamethoxazole for patients > 2 months
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# whooping Postexposure Prophylaxis
Given to **every household contacts** within 21 days of the onset of cough in the positive patient, whether they have been vaccinated or not Erythromycin 500 mg PO 4 times daily x 14 days Erythromycin 10 mg/kg PO 4 times daily x 14 days Alternative antibiotics: Clarithromycin and Azithromycin Azithromycin is preferred for infants < 1 month of age
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