CCP 345 Respiratory Emergencies Flashcards
Retropharyngeal Abscess in Pediatric patients
- This is a potentially life-threatening emergency in young children with signs of upper airway obstruction or meningismus
- Retropharyngeal abscess is often related to oral trauma.
- Retropharyngeal abscess is most frequently caused by: Staphylococcus aureus, group A streptococci, and anaerobes
- Treatment is admission, IV antibiotics and, for more severe cases, surgical drainage
pediatric respiratory distress vs respiratory failure
Respiratory failure is identified by the presence of extreme distress, hypoventilation or hyperventilation, altered mental status, pale, mottled or cyanotic skin color, and/or hypotonia
define Stridor
- sound associated with upper airway obstruction
- harsh vibratory sound of variable pitch caused by partial airway obstruction or collapse → turbulent airflow through upper airway
- Stridor is described by timing in the respiratory cycle (inspiratory, expiratory, biphasic) and quality (coarse or high-pitched).
define Inspiratory stridor
stridor d/t pathology above the glottis
define biphasic stridor
stridor d/t pathology at the glottis
define expiratory stridor
stridor d/t pathology below the glottis
What the typical pathogens in epiglottitis?
- Epiglottitis may be caused by many bacteria or local injury.
- In the post–H. influenzae type b vaccine era, the typical profile of epiglottitis has changed to include older patients
Haemophilus influenza B, A, F, nontypeable)
Strep
Staph
Pseudomonas
Candida
Non-infectious causes – thermal burns, chemical burns, allergic rxn, foreign bodies
describe the management of epiglottitis
Stable patient:
- Infants and children: A stable patient who is maintaining a patent airway and adequate oxygenation should not be moved or repositioned for examination, laboratory tests, or radiography. Such patients should be carefully transported to a setting where definitive airway management can be achieved in a controlled fashion, generally the operating room
- Adolescents and adults = have more real estate and rarely require airway management. They should be observed in the ICU and given IV abx
Unstable patient (respiratory failure):
- Get help! (anesthesia, ENT, gensx)
- Start with BVM and prepare for intubation
- Have a backup plan – needle ventilation / cut to air
Patients often remain intubated for 3 to 5 days in order for antibiotic therapy to reduce inflammation and surrounding tissue edema
define Mild Croup
Stridor at rest or only when agitated
No tachypnea
No retractions
No Mental Status Changes
define Moderate Croup
Stridor at rest
Mild tachypnea
Mild retractions
No mental status changes
define Severe Croup
Stridor at rest
Respiratory distress
Severe retractions
± Mental status changes present
Define TTN and identify the population most at risk for it
- benign, self-limited condition that can present in infants of any gestational age shortly after birth
- caused by a delay in the clearance of fetal lung fluid after birth → ineffective gas exchange, respiratory distress, tachypnea
- Maternal risk factors: delivery before completion of 39 weeks gestation, a cesarean section without labor, gestational diabetes, and maternal asthma
- Fetal risk factors: male gender, perinatal asphyxia, prematurity, small for gestational age, and large for gestational age infants
- Incidence is inversely proportional to gestation delivery age: 10% of infants 33-34 weeks, 5% 35-36 weeks, <1% in term infants
Detail the pathophysiology of TTN
- Caused by ineffective absorption of fetal lung fluid
- Passive movement of sodium through epithelial sodium channels (ENaC) is believed to be the principle mechanism of reabsorption of fetal lung fluid
- With the onset of labor, maternal epinephrine and glucocorticoids activate the ENaC on the apical membranes of type II pneumocytes
- Failure or delay in clearance of intra-alveolar fluid in patients with TTN is due to:
- Lack of ENaC expression or activity
- Lack of active labor and its associated hormonal changes
- Ineffective lung distention and lack of alveolar air interface
- Immaturity of ENaC
- Especially relevant in the late preterm infant
Ok so this all sounds like a bunch of complicated bullshit, and it is, but basically what it boils down to is when the baby is floating around in the womb it has a bunch of fluid in its lungs. When the baby gets born normally, there’s a bunch of biochemical shit that happens that causes the lung fluid to get re-absorbed/washed out. If the kid gets born premature/c-section/whatever there isn’t the trigger to wash out the fluid in the lungs and he gets this shitty lung water that causes respiratory distress
Summarize & describe the clinical manifestations of TTN
- Clinical presentation is reflection of decreased lung compliance associated with pulmonary edema and ineffective fetal lung fluid clearance
- Onset: Present very early after birth
- Duration: 2- 3 days
Tachypnea (RR >60) Nasal flaring Grunting Intercostal/subcostal/suprasternal retractions Crackles on auscultation Mild degrees of hypoxia
Define neonatal RDS and identify the population most at risk for it
- common cause of respiratory distress in a newborn
- presents within hours after birth, most often immediately after delivery
- occurs from a deficiency of surfactant, d/t either inadequate surfactant production, or surfactant inactivation (MAS)
- inversely proportional to the gestational age of the infant, with more severe disease in the smaller and more premature neonates
- The most important risk factors are prematurity and low birth weight
Detail the pathophysiology of Neonatal RDS (Respiratory Distress Syndrome)
- RDS affects premature neonates, born before the lungs start producing adequate surfactant
- RDS commonly occurs below 32 weeks
- CXR shows a “ground-glass” appearance
- Inadequate surfactant → high surface tension within alveoli → atelectasis → inadequate gas exchange → hypoxia, hypercapnia and respiratory failure
Explain surfactant, its chemical composition and how it helps with lung compliance and the factors that affect its production (Gestational age, Meconium aspiration syndrome, Steroid administration prior to delivery)
- mixture of lipids and proteins which is essential for gas exchange at the fluid−air interface of the internal lung surface
- hydrophobic and hydrophilic properties cause ↓ surface tension, thus keeping the alveoli open during the respiratory cycle
- begins to be produced in the fetus at about 24 to 28 weeks of pregnancy. By ~35 weeks gestation, most babies have adequate amounts of surfactant
- Pulmonary surfactant gets inactivated in babies who have MAS
- surfactant after birth prevents/treats neonatal RDS in preterm delivery
- Antenatal steroids for preterm labour ↑ the production of surfactant
Summarize and describe the clinical manifestations of RDS
- Signs of RDS appear within 4hr of birth
- tachypnea (>60 breaths/min), intercostal + subcostal retractions, nasal flaring, grunting, and cyanosis
- Tachypnea is d/t an attempt to ↑ Ve to compensate for a ↓ Vt and ↑ dead space
- Retractions occur as the infant is forced to generate a ↑ intrathoracic pressure to expand the poorly compliant lungs.
- The typical CXR shows low lung volumes and a bilateral, reticular granular pattern (ground glass appearance) with superimposed air bronchograms. In more severe cases, there is complete “white out” of the lung fields.
General management for RDS
- Avoid hypoxemia and acidosis
- Optimize fluid management: avoid fluid overload and resultant body and pulmonary edema while averting hypovolemia and hypotension
- Reduce metabolic demands and maximize nutrition
- Minimize lung injury secondary due to volutrauma and oxygen toxicity
Antenatal corticosteroids (in an expected preterm birth)
Monitoring oxygenation and ventilation
Assisted ventilation of the neonate
Exogenous surfactant therapy
Supportive care, including thermoregulation, nutritional support, fluid and electrolyte management, antibiotic therapy, etc
define and describe BLES surfactant
- BLES = bovine lipid extract surfactant
- natural extract of cow pulmonary surfactant
- commonly used to treat RDS in premature infants in NICUs
- studies show improved outcomes w/ animal‐derived surfactants vs synthetic products
Which pathogens are associated with croup?
- Human parainfluenza virus (HPIV) = 50% to 75% of cases
2. RSV, influenza A/B, and rhinovirus = remainder
define MAS (Meconium Aspiration Syndrome) and identify the population most at risk for it
- Meconium = 1st stool of newborn. sometimes meconium passed in uterus
- MAS = neonatal respiratory distress w/ meconium-stained amniotic fluid (MASF)
- can be mild distress to respiratory failure
- MSAF is more common in POST-term newborns
Detail the pathophysiology of MAS
💵💵💵MONEY SLIDE💵💵💵
- Meconium passage
- Aspiration (MSAF inhalation by the fetal airway)
- Airway obstruction (meconium in the airways → meconium plugging → atelectasis)
- Inflammation (meconium triggers inflammatory processes → chemical pneumonitis)
- Surfactant inactivation: (Inflammation → Surfactant inactivation → increased surface tension w/ ↓ compliance, and ↓ oxygenation)
Summarize and describe the clinical manifestations of MAS
- Evidence of meconium-stained amniotic fluid (MSAF)
- Perinatal asphyxia. These infants have neurologic and/or respiratory depression at birth typically due to hypoxia or shock
- Fetal growth restriction and postmaturity – Affected infants are frequently small for gestational age and born postterm
- Infants with MAS typically have respiratory distress with marked tachypnea and cyanosis immediately after birth → increased respiratory rate and use of accessory respiratory muscles of respiration demonstrated by intercostal and subxiphoid retractions and abdominal (paradoxical) breathing, often with grunting and nasal flaring
- Affected infants typically have a barrel-shaped chest with an ↑ A/P diameter caused by overinflation. Auscultation reveals rales and rhonchi
- In patients with severe MAS, pneumothorax and pneumomediastinum are common findings and other less common air leak syndromes can occur
Define Early-onset neonatal pneumonia and identify the populations most at risk for it
- Early-onset pneumonia (≤3 days), which is generally acquired from the mother during labor or delivery.
- Early-onset bacterial pneumonia is most commonly caused by group B streptococcus.
- Risk factors associated with early-onset pneumonia include prolonged rupture of the fetal membranes (>18 hours), maternal amnionitis, preterm delivery, fetal tachycardia, and maternal intrapartum fever
- Early-onset pneumonia commonly presents with respiratory distress beginning at or soon after birth.
- other clinical manifestations include temperature instability, apnea, lethargy, tachycardia, poor perfusion, tachypnea, and poor feeding.
Define Late-onset neonatal pneumonia and identify the populations most at risk for it
- Late-onset pneumonia (>3 days of age) is typically due to nosocomial organisms from previous colonization of the infant or transmission from care providers or contaminated equipment
- Late-onset disease is associated with mechanical ventilation, airway anomalies, prolonged hospitalization, and aspiration of gastrointestinal contents due to neurologic impairment
- clinical manifestations include temperature instability, apnea, lethargy, tachycardia, poor perfusion, tachypnea, and poor feeding
why are neonates prone to developing pneumothorax?
- Lack of surfactant makes premature lungs stiff and fragile.
- The baby who requires BMV is at risk of having iatrogenic PTX (why we need to pay attention to the pressure that we are using)
describe Tranillumination for pneumothorax
- Place light source (otoscope, transilluminator) on infant’s chest. Ensure it isn’t hot.
- A normal chest will have a small glowing “Halo” around the light source. Usually it extends less than 1 cm from the light source and is symmetric.
- If the chest “lights up like a jack-o-lantern (large area of redness that is often asymmetric), then PTX should be HIGH on your DDx list.
- You should compare to the other side if you are unsure.
describe “Aspiration of pneumothorax” in the neonate
- Traditionally used to relieve tension PTX.
- In small children and neonates, may be the definitive procedure for simple PTX.
- More compliant chest wall and elastic tissues in kids may allow for the hole to spontaneously seal after the procedure so that you don’t have to follow it up with a traditional chest tube.
- If the PTX re-accumulates after aspiration, then a thoracostomy tube will need to be placed
- Locate 2nd or 3rd intercostal space at the midclavicular line
- Prep skin with antiseptic and provide analgesic and anesthetic
- Advance needle perpendicularly over superior border of rib while aspirating. Having saline in syringe will allow you to detect when you’ve entered the ptx.
- When bubbles are present or you have free movement of the syringe plunger, evacuate the pneumothorax.
- A 3-way stopcock can be placed between syringe and butterfly needle, which will allow for controlled evacuation of pneumothorax.
define Tracheoesophageal Fistula (TEF) + detail pathophysiology
- Tracheoesophageal fistulas (TEFs) represent one of the most common congenital anomalies seen in major pediatric surgical centers
- TEF occurs d/t abnormal septation of the caudal foregut during the fourth and fifth weeks of embryonic development
- Under normal conditions, the trachea forms as a diverticulum of the foregut and develop a complete septum that separates it from the esophagus.
- Fistula formation in conjunction with esophageal atresia (EA) occurs during an abnormal posterior positioning of the tracheoesophageal septum, resulting in a retained connection between trachea and esophagus.
Summarize and describe the clinical manifestations of Tracheoesophageal Fistula (TEF)
- clinical presentation of TEF depends upon the presence or absence of esophageal atresia (EA).
- In cases w/ EA (95 percent), Infants w/ EA become symptomatic immediately after birth, with ↑ secretions → drooling, choking, respiratory distress, and inability to feed.
- A fistula between trachea and distal esophagus → gastric distension. Reflux of gastric contents through the TEF → aspiration pneumonia and ↑ morbidity
define Congenital Diaphragmatic Hernia (CDH)
- Congenital diaphragmatic hernia (CDH) is a condition resulting from a developmental defect in the diaphragm → protrusion of abdominal contents into the thoracic cavity
Detail the pathophysiology of Congenital Diaphragmatic Hernia (CDH)
- The septum transversum and pleuroperitoneal membranes are the main components in the development of the diaphragm
- Any disturbance in the formation of the pleuroperitoneal membranes can → diaphragmatic discontinuity and CDH
- The associated herniation of the abdominal viscera into the thoracic cavity can interfere with normal lung development and forms the basis for the two main pathological findings noted in CDH - lung hypoplasia and abnormal pulmonary vascular development
- Lung hypoplasia is reflected by a marked ↓ in the airway generations, terminal bronchioles, and alveoli. The hypoplasia is noted bilaterally with the lung on the same side of the defect affected more severely than the other lung. There is also an abnormal vascular remodeling of the pulmonary vasculature resulting in the thickening of the arterial medial walls with the potential to develop persistent pulmonary hypertension (PH)
- Left ventricular hypoplasia and dysfunction, which can worsen the PH, are also noted in CDH
TL;DR genetic shit causes the baby to have a fucked up diaphragm while in mom. D/t the fucked up diaphragm the abdominal contents get pushed up and fuck up lung development. These fuck up lungs → fucked up bronchioles, PH and infants with CDH most often present with respiratory distress in the first few hours or days of life
Summarize & describe the clinical manifestations of CDH
- respiratory distress in the first few hours or days of life.
- usually acute respiratory distress at birth
- degree of respiratory distress is dependent on the severity of lung hypoplasia and pulmonary hypertension (PH)
- Adrenal insufficiency a common finding
- Physical findings include a barrel-shaped chest, a scaphoid-appearing abdomen (d/t loss of the abdominal contents into the chest), and absence of breath sounds on the ipsilateral side
Discuss the typical treatment plan for a patient with CDH
- Intubation and ventilation
- low PIP (PIP, goal <25 cm H2O) to minimize lung injury
- NG tube w/ continuous suction to decompress abdominal contents and ↓ lung compression
- UA line for frequent monitoring of ABG and blood pressure (BP), and UVC for administration of fluids + medications
- BP support to maintain MAP ≥40 mmHg to minimize any right-to-left shunting
Define BPD (Bronchopulmonary Dysplasia), the severities of BPD in the neonatal population born < 32 weeks and the neonatal population born > 32 weeks
- The terms bronchopulmonary dysplasia and chronic lung disease of prematurity are used synonymously in practice and in the literature
- Bronchopulmonary dysplasia is best thought of as a syndrome of lung immaturity, injury and inflammation, and a dysmature or dysregulated repair response, which → a persistent oxygen dependence and respiratory issues
- Infants with birth weights (BW) <1250 g account for 97 percent of the cases of BPD. For extremely preterm (EPT) infants (gestational age [GA] <28 weeks), the incidence of BPD is approximately 40 percent, and the risk ↑ with decreasing GA
define and detail BPD
disruption of fetal/neonatal lung development and injury d/t inflammation and damage from antenatal factors (intrauterine growth restriction, maternal smoking) and/or postnatal factors (eg, mechanical ventilation, oxygen toxicity, and infection)
Summarize and describe the clinical manifestations of BPD
- Infants with BPD usually are tachypneic
- Depending upon the extent of pulmonary edema and/or atelectasis, they may have mild to severe retractions, and scattered rales may be audible.
- Intermittent expiratory wheezing may be present in infants w/ airway narrowing from scar formation, constriction, mucus retention, collapse, and/or edema
- As BPD evolves, the CXR also changes from clear lung fields to findings that include diffuse haziness and a coarse interstitial pattern, which reflect atelectasis, inflammation, and/or pulmonary edema
- Patients with more severe BPD are hypoxemic and hypercapnic and typically require mechanical ventilation and oxygen supplementation.
- They have abnormal pulmonary function including ↓ tidal volume, ↑ airway and vascular resistance, and ↓ dynamic lung compliance and uneven airway obstruction resulting in gas trapping and hyperinflation with abnormal distribution of ventilation
