2160 Unit 4 Test Review

Diagnosis and treatment of Choanal Atresia?

-Cyanosis that resolves with crying or an open mouth. -Inability to pass a catheter through nares into the nasal pharynx. -Signs such as chronic unilateral rhinorrhea, w/o frank resp distress. Treatment: -Surgery.

Tetralogy of Fallot

1. Pulmonary artery stenosis 2. Ventricular Septal Defect 3. Overriding aorta to the right 4. Right ventricular hypertrophy

Omphalocele

1/3 have trisomy 13, 18, 21. Prenatal diagnosis - increased alpha-feroprotein level

Bochdalek hernia

90% on the left side

Pulm Hemorrhage prevention and treatment

Antenatal corticosteroids Prevent PDA HFOV -Resuscitation -Ventilation -Surfactant -Echocardiogram if PDA

Pulm hemorrhage clinical presentation and diagnosis

Between 2nd-4th day of life. Sudden deterioration -Pallor (pale) -Cyanosis -Bradycardia -Apnea -Pink/red frothy secretions -CXR, white out w/ just an air bronchogram visible. -CBC and coagulation studies. -Echocardiogram to exclude hemodynamically significant PDA

Symptoms and treatment of Pneumothorax?

Chest pain and SOB. Treatment: -Thoracentesis -Chest tubes -Pleurodesis -Thoracotomy

PPHN clinical presentation and diagnosis

First 12 hours of life. -Cyanosis -Tachypnea -Hypoxia that's refractory to O2 -Retractions -Grunting -Nasal flaring The recognition of risk factors for PPHN, such as MAS is one of the major diagnostic tools to differentiate babies with PPHN from those with structural heart disease, keeping in mind that idiopathic PPHN can present without signs of acute perinatal distress.

Air leak syndrome prevention, treatment, complications, prognosis

Gentle ventilation, low everything w/ high rate. -Needle aspiration -Chest tube drainage -HFJV Prognosis depends on underlying condition, severe syndromes are associated with risk of IVH and death.

Gastroschisis

Herniates to the right side of the umbilicus.

*RDS*

Incidence 60-80% *in premies*

Epiglottitis

Inflammation of the epiglottis, often results from bacterial infection and may lead to airway obstruction, especially among children -High fever -Severe sore throat -Dysphagia (difficulty swallowing) with drooling -Cough progressing to stridor -Muffled voice -Cyanosis -Retractions -Nasal flaring -Bradypnea -Dyspnea -Swollen epiglottis (Thumb sign) -Antibiotics -Mechanical ventilation

Macroglossia

Macroglossia is the medical term for an unusually large tongue.

Describe the complications of treatment of RDS

Metabolic and cardiac functions are affected. -Death most often associated with pulmonary interstitial emphysema, pneumothorax, IVH.

What ABGS would you expect to see in severe RDS?

Moderate to severe hypoxemia, varying degree of hypercapnia and respiratory acidosis.

Pulm Hemorrhage Complications and prognosis

Mortality rate is 50%. Babies that survive are at risk for every type of resp failure.

Ventricular Septal Defects (VSD)

Most common congenital heart defect. Left-right shunt. Surgery and therapy.

Aortic Stenosis (AS)

Narrowing of the aortic valve orifice itself Valvular is most common Clinical presentation depends on severity, if not treated it may present in cardiogenic shock with hypotension, poor perfusion, and metabolic acidosis. -Emergency therapy -Prostaglandin E1 -Surgical repair

Necrotizing Enterocolitis (NEC)

Occurs in premature and newborn infants. Thought to be infection and or ischemia of the gut, deadening of the intestines. -90% of cases are in newborns -Diagnosis: If stool is bloody/greasy, hard stomach Treatment: Withholding feedings, administering antibiotics, blood transfusions, surgery

Chest wall malformations

Pectus excavatum Pectus carinatum -Asphyxiating thoracic dystrophy -Scoliosis and kyphoscoliosis

RDS cause

Surfactant deficiency

*Bronchopulmonary Dysplasia* clinical presentation and diagnosis

The development of BPD is often suspected when mechanical ventilation and oxygen dependence extend beyond 10-14 days, and can be determined by using a web based calculator by the NICHD. Diagnosis is based on clinical and radiographic manifestations. You have to rule out congenital heart disease, pulmonary lymphangiectasia, chemical pneumonitis resulting from recurrent aspiration, CF, and inherited surfactant protein deficiencies.

Sign and Symptoms of Atelectasis?

Varies with cause and severity. -Dyspnea -Cyanosis -V/Q mismatch -Tachypnea -Nasal flaring -Retractions -Grunting -ABG shows low sats, normal PaCO2. -Chest pain on deep inspiration

MAS prevention and treatment

-Don't deliver late -Close intrapartum monitoring for hypoxia/distress -Don't stimulate -Supplemental O2 (95-99%, PaO2 60-80.) -Mechanical ventilation -High frequency ventilation -Surfactant therapy -Inhaled NO -ECMO -Cardiovascular support -Steroid therapy

What are signs and symptoms of ARDS?

-Dyspnea -Cyanosis -Bilateral crackles -Tachypnea -Tachycardia -Diaphoresis -Use of accessory muscles -Systemic hypotension -Cough -Chest pain

What is the treatment for BPD?

-Lung protective ventilator strategies -O2 therapy -Antioxidants -Inhaled NO -Nutrition -Corticosteroids -Methlyxanthines

Bronchopulmonary Dysplasia prevention

-Lung protective ventilator strategies -O2 therapy -Antioxidants -Inhaled NO -Nutrition -Corticosteroids -Methylxanthines

RDS Clinical presentations and diagnosis

-Tachypnea -Grunt -Nasal Flaring -Retractions -Cyanosis -L/S ratio (>2.0)

Transient tachyonea prognosis and complications

Self resolves, complications are rare, though air leaks may occur.

Etiology of RDS

Associated with the deficiency of pulmonary surfactant and abnormal lung surface tension properties. Characterized by decreased FRC, decreased pulmonary compliance, increase in pulmonary resistance, v/q mismatch. Can result in hypoxia, hypercapnia, respiratory acidosis, and reduced pulmonary blood flow.

Eisenmenger Syndrome

At birth, shunts flow in a left to right direction; eventually, there will be increased blood in the pulmonary circulation, leading to pulmonary hypertension. this will reverse the shunt from right to left, causing cyanosis, RVH, polycythemia, clubbing.

Diagnosis and treatment for Epiglottitis vs. Croup?

Epiglottitis: Diagnosis: Must be assumed based off clinical manifestations. Ex: Stridor, barking cough, fever, hoarse voice, etc. Treatment: Establishment of stable artificial airway, mechanical ventilation may be needed for a short time if heavy sedation is required. -2 day course of ceftriaxone as effective as 5 days of chloramphenicol. Croup, aka laryngotracheobronchitis: Diagnosis: Lateral neck radiograph, shows a large retropharyngeal air shadow without epiglottic swelling. Shows classic "steeple" sign, narrowing of the trachea. Treatment: Temp control, adequate hydration, and humidification of inspired air. Cool mist tents, nebulized racemic epi 2.2% dilution w/ 0.5-1.0 mL of medication, diluted to 3mL volume w/ NS.

Atrioventricular Septal Deflect (ASVD)

Partial AVSD's are characterized by a primum ASD and common AV valve, but there is no defect in the ventricular septum. Complete AVSD's are characterized by abscence of the of a portion of the atrial septum and the ventricular septum. Left-right shunting. -Respiratory distress -Pulmonary edema -Growth failure -CXR shows cardiomegaly and increased pulm vascular markings. Most common in infants with down syndrome (Trisomy 21) Surgical repair.

RDS complications

Persistent PDA, bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, NEC.

Neonatal apnea clinical presentation and diagnosis

Presents 2-3 days after birth. Apnea is generally diagnosed with continuous carido-respiratory monitoring.

PPHN treatment

To reverse hypoxemia, improve pulmonary and systemic perfusion, and minimize hypoxic-ischemic end organ injury. 1. General management : Maintenance of normal temp, electrolytes, glucose, hemoglobin, and intravascular volume. -Acidosis worsens PVR, should be corrected by normalizing gas exchange and using sodium acetate in IV fluids to improve metabolic acid-base derangements. 2. Minimal handling : Infants with PPHN are very liable wit significant deterioration after seemingly minor stimuli. ETT suctioning only when indicated, noise and physical manipulation should be minimized. 3. Supplemental O2 : Bc hypoxia is a potent pulmonary vasoconstrictor. Preductal sats should be 90-99% 4. Mechanical ventilation : To improve oxygenation and improve ABG. Sats should be 90-99%, PaCO2 40-50, and pH 7.35-7.40. -Nitric oxide, phosphodiesterase inhibitors, prostacylin analogs, sedation and analgesia. -Maintanence of cardiac output and systemic BP. -ECMO

Neonatal Apnea treatment, complications, prognosis

Xanthines derivatives CPAP and NIPPV Mech vent Blood transfusions AOP doesn't alter an infant's prognosis unless severe, recurrent, or refractory to therapy.

Clinical signs of and treatment for IVH?

*ASK*

When does IVH occur mostly in neonates?

*ASK*

RDS Prevention and Treatment

-Avoid poorly timed c-section -Antenatal and intrapartum fetal monitoring -Antenatal steroid therapy Treatment: -Surfactant -O2 therapy -CPAP -Mechanical vent

Initial signs of fetal asphyxia?

-*Low O2* Not breathing or very weak breathing. Skin color that is bluish, gray, or lighter than normal. Low heart rate. Poor muscle tone. Weak reflexes. Too much acid in the blood (acidosis) Amniotic fluid stained with meconium (first stool) Seizures.

What is the possible treatment of ARDS?

-Corticosteroids -O2 therapy -Lung expansion -Mechanical vent -Inhaled NO -ECMO -Prone vent -ARDS net

Air leak syndrome clinical presentation and diagnosis

-Cyanosis -Hypotension -Hypoxemia -Hypercapnia -Resp acidosis -Diminished breath sounds -CXR -Transillumination -Needle aspiration -Electrocardiogram

MAS clinical presentation and diagnosis

-Cyanosis -Respiratory Distress -Grunting -Retractions -Nasal flaring -Tachypnea -Yellow stained skin/nails Diagnosis: -Chest ausculatation reveals rales and diminished. -CXR shows patchy areas of atelecatsis caused by obstruction, hyperexpansion, flattening diaphragm, air leaks, pneumothorax, and pneumomediastinum.

What is the treatment for increased ICP?

-Head elevation -Hyperventilation -Osmotic diuretics -Corticosteroids -Hypothermia -Ventilatory maneuvers -Staticus epilepticus

Clinical features of increased intracranial pressures?

-Headache -Diplopia -Strabismus -Papilledema -Herniation

Monitoring and resp care of patients with cardiac abnormalities.

-Hemodynamic monitoring -Pulse ox -Capnography -Cardiac output monitoring -Ventilator management -Inhaled nitric oxide therapy -Gas mixtures to increase pulmonary vascular resistance

Symptoms and treatment of Diaphragmatic Hernia?

-Most often on the left side, after birth: Hypoxia, hypercapnia, and acidosis develop causing constriction of the arterioles and exacerbation of pulmonary hypertension and persistent fetal circulation. -All lung tissue is hypoplastic , including the pulmonary vasculature, even on the "good" side. Treatment: -Surgery

Bronchopulmonary Dysplasia treatment

-Oxygen -Mechanical ventilation -Fluid management -Drug therapies -Nutrtion -Social issues

Protocols

-Oxygen therapy protocol to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. -Airway clearance therapy (Bronchial hygiene therapy) to enhance the mobilization of airway secretions. -Lung expansion therapy to attempt to offset the alveolar consolidation and atelectasis. -Mechanical ventilation protocol is usually needed to provide and support alveolar gas exchange and eventually return patient back to spontaneous breathing.

Transient tachypnea differential diagnosis

-RDS -Sepsis -Pneumonia -PPHN -Hyperventilation as respiratory compensation for a metabolic acidosis

Treatment of MAS?

-Supplemental O2 therapy. -Mechanical ventilation -High frequency ventilation -Surfactant therapy -Inhaled nitric oxide -ECMO -Cardiovascular support -Steroid therapy

What is the treatment for RDS?

-Surfactant therapy -Oxygen therapy -CPAP -Mechanical ventilation

Bronchopulmonary Dysplasia complications

-Tachypnea -Retractions -Dyspnea -Cough -Wheezing. -Cardiac complications

Treatment of Pneumonia?

Based on specific case and severity of symptoms -Bacterial: First line is antibiotics -Fungal disorders: Antifungal agents -Viral: Antiviral meds -O2 therapy -Lung expansion therapy -Airway clearance therapy -Thoracentesis (if pleural effusion is present)

A premature infant born at 24 weeks of gestation suffers immediate respiratory distress in the delivery room. She is intubated and given endotracheal surfactant replacement immediately. Despite the surfactant therapy and mechanical ventilation, she continues to have respiratory distress. Her chest radiograph demonstrates air in the right pleural space that persisted despite placement of two chest tubes (see Figure 32-4 in text). The persisting air leak into the pleural space is likely from either tracheal trauma from intubation or pleural disruption from chest tube insertion in addition to hyaline membrane disease (respiratory distress syndrome) and mechanical ventilation.

Because her air leak has persisted despite chest tube placement, the next most appropriate intervention is: A. Rigid bronchoscopy B. Alteplase instilled in the pleural space C. Pneumonectomy D. Chest tube replacement Answer: D When the integrity of the lung is not reestablished after an air leak or injury, a large portion of the volume of inspired gases may pass directly through the air leak, thus bypassing the gas-exchanging units of the lung. Chest tube replacement may be needed.

Lung bud abnormalities

Bronchogenic cyst Congenital cystic adenomatid malformation Pulmonary sequestration Congenital lobar emphysema

Diagnosis of PPHN?

Chest xray ABG will show hypoxemia Echocardiography

Choanal atresia

Choanal atresia is a congenital narrowing of the back of the nasal cavity that causes difficulty breathing. -Obligate nasal breathers -Unilateral is most common -Bilateral is neonatal emergency -Oral airway

*Pulmonary hemorrhage*

Discharge of bloody fluid from the upper respiratory tract or the ETT. Fulminant lung edema with leakage of red blood cells and capillary filtrate into the lungs. -More than 80% has RDS -23 to 28 weeks gestation

PPHN Complications and prognosis

High frequency ventilation, nitric oxide, and ECMO has significantly improved survival rates. Mortality rates are still high 10%, if they survive they're still at high risk for neurodevelopmental delays.

RDS prognosis

In milder cases, S/S peak within 72 hours, followed by gradual improvement. Severely affected infants may die within the first week, death often associated with pulmonary interstitial emphysema, pneumothorax, or IVH. Immature lungs, metabolic and cardiac function affected.

Contraction of the Aorta

Increased LV afterload, severe narrowing of the thoracic aorta. Same presentations as AS. -Emergent opening of the PDA using PGE1 infusion, mech vent, and diuresis of the pulm edema that results from left atrial hypertension.

Atrial Septal Defect (ASD)

Left-right shunt. Surgical repair

What are contributing factors to infants developing RDS?

Low birth weight, premature. -Factors in mom: Diabetes, multiple births, c-section, precipitous deliveries, fetal asphyxia, cold stress, history of previous affecting infants. Higher in Caucasian and male infants.

Transient tachypnea treatment

Maintain adequate oxygenation and ventilation. 40-60 breaths/min -Supplemental oxygen -No feeding if breaths are 60-80 per min, gavage feedings/IV fluids. -Broad spectrum antibiotics

Mandibular hypoplasia

Mandibular hypoplasia (MH) is a condition, which characterizes deviation in the mandibular growth patterns causing functional and esthetic alterations.

*Neonatal pneumonia* incidence, modes of transmission, and risk factors.

Modes of transmission: Intrauterine, ascending vertical transmission, post natal (Nosocomial or community acquired.) Risks: -Poor teenage mothers -Prolonged ruptured membranes -Maternal peripartum fever, GBS in mom, UTI, chorioamnionitis. -Meconium stained fluid -Resuscitation at birth -Multiple gestations

Diagnosis and treatment of Bronchioloitis?

Nasopharyngeal aspirate or nasal lavage provides samples of the virus. Diagnosis is based off clinical manifestations and the results from the viral culture and antigen detection assays. Treatment: -Supplemental O2 therapy -Intravenous hydration -Mechanical vent -Nebulized hypertonic saline 3% -Corticosteroids sometimes -Albuterol as needed -Ribavirin

What are clinical signs of Pleural Effusion? What is the treatment for Pleural Effusion?

Pleural Effusion: -Decreased breath sounds -Chest pain -Chest wall tenderness -Pain w/ coughing -Pain w/ deep breathing -Dull percussions -Crackles Treatment: -Thoracentesis -Chest tube -VATS (Video assisted thoracoscopic surgery)

Transient tachypnea incidence, pathophsyiology, and risk factors

Relatively benign, self limited condition *(self resolves)* Between 37-42 weeks of gestation. *Happens only in full term babies* Risks: -C section w/o labor -Male gender w/ asthmatic mother -Macromasia (big baby) -Multiple gestations -Excessive sedation/large amounts of IV fluids to mom -Delayed cord clamping

*PPHN* incidence, cause, and pathophysiology.

Risk factors: -Late preterm infants -Black race -Large for gestational age -Small for gestational age -Moms w/ diabetes, obesity, or advanced age. Can be idiopathic or secondary to -Intrapartum asphyxia -Infection -Pulmonary hypoplasia -Congenital heart disease -MAS -RDS -Drug therapy PPHN is characterized in 3 types: 1. Maladaption - Structurally normal but but abnormally constricted pulm vasculature caused by diseases like RDS, MAS, pneumonia. 2. Excessive muscularization - Lung w/ normal parenchyma but remodeled pulmonary vasculature characterized by smooth muscle cell thickness and distal extension of muscle to vessels that are usually nonmuscular. Hypoplastic vasculature - Associated with underdevelopment of the pulmonary vasculature, as seen in congenital diaphragmatic hernia.

*Air leak syndromes* incidence, cause, pathophysiology.

Risk for air leaks is higher in infants with RDS, MAS, and pulm hypoplasia, and infants that need resuscitation at birth. PPV, CPAP, mech vent increase incidence for air leaks.

What causes Bronchopulmonary Dysplasia?

Severe chronic lung injury in premature infants who survived hyaline membrane disease after mechanical ventilation, is most common long term complication. -Volutrauma -Barotrauma -O2 toxicity to lungs during mechanical ventilation for treatment of RDS -Airway injury -Bronchial smooth muscle hypertrophy -Peribronchial inflammation -Parenchymal fibrosis. -Prematurity -Hypoxia or hyperoxia induced lung injury -Vent induced lung injury -Inflammation -Nurtrition -PDA -Genetics -Vascular

Patent Ductus Arteriosus

The PDA typically connects the pulmonary with the systemic circulation, and most blood passing into the PA in utero shunts from the pulmonary artery and into the ascending aorta. Clinical presentations of PDA include tachypnea, tachycardia, and a continuous murmur. May manifest cardiomegaly, pulmonary congestion, and failure to thrive.

A 7-year-old girl complains of cough, right-sided chest pain, and fever. She has previously been well. Examination by her pediatrician reveals inspiratory crackles over the right lower lobe, so amoxicillin is prescribed for presumed bacterial pneumonia. Two days later her fever has persisted and she is increasingly short of breath. A chest radiograph (see Figure 32-1) demonstrates a right lower lobe infiltrate with right-sided pleural effusion. The right-side-down lateral decubitus radiograph (see Figure 32-2) confirms the effusion. Video-assisted thoracoscopic surgery (VATS) is performed to sample the pleural effusion and place a chest tube for drainage. Analysis of the pleural fluid reveals a white blood cell count of 22,000 per cubic mm with 96% segemented neutrophils. The total protein is 5.4 mg/dl and the lactate dehydrogenase (LDH) is 425 IU. Although the Gram stain and culture of the fluid is negative, a blood culture is positive for Streptococcus pneumoniae. In addition to chest tube drainage she is treated with intravenous ampicillin. After 3 days the chest tube is removed and she completes a 10-day course of intravenous ampicillin followed by 7 days of oral amoxicillin. She makes a full recovery and her chest radiograph returns to normal.

The most appropriate label for this patient's pleural fluid is: A. Empyema B. Chylothorax C. Hemothorax D. Transudative effusion Answer: A The pleural fluid qualifies as an empyema because the white cell count is greater than 15,000 per cubic mm. It is not a chylothorax because the cells are not predominantly lymphocytes. It is not a hemothorax because there is no gross blood mentioned in either the visual description of the fluid or in the cell count analysis. The protein and LDH are too high for this to be a transudate, and in fact, it is an exudative effusion.

Upper airway disorders.

This includes the nose, nasal choanae, nasopharynx, mouth, oropharynx, and structures of the larynx. Supralaryngeal obstruction: -Choanal atresia -Pierre robin syndrome -Deep neck infections -Tonsillar enlargement -Peritonsillar abcess -Retropharyngeal abcess -Obstructive apnea Periglottic Obstruction: -Epiglottitis -Laryngotracheobronchitis -Traumatic and postop laryngotracheobronchitis

Transient tachypnea clinical presentation and diagnosis

Typically presents with tachypnea and cyanosis within the first few hours after birth. -Nasal flaring, grunting, retractions. -ABG shows mild to moderate hypoxemia, hypercapnia, respiratory acidosis. -CXR may show pulmonary vascular congestion, prominent perihilar streaking, fluid in the interlobular fissures, hyperexpansion, flat diaphragm. -Mild cardiomegaly and pleural effusions may be present.

Hypoplastic Left Heart Syndrome

Underdevelopment of the left side of the heart. Most extreme end of the spectrum. -Systemic blood flow depends on patent foramen ovale. Premature closure of the PDA results in hypoperfusion, metabolic acidosis, circulatory collapse, and death. -Surgical repair, Norwood-Glenn-Fontan -Subambient O2 concentrations

*Neonatal Apnea*

Unexplained episode of cessation of breathing for 20 seconds or longer. Apnea of prematurity (AOP) - Cessation of breathing for 20 seconds, or is accompanied by bradycardia or cyanosis in an infant younger than 37 weeks postmenstrual age. Apnea of infancy (AOI) - Infants over 37 weeks postmenstrual age or more with onset apnea Sudden Unidentified Infant Death Syndrome - Sudden death of an infant less than 1 year of age that remains unexplained. Apnic spells usually begin at 1 or 2 days after birth.

What are signs and symptoms of pneumonia?

Viral: Coryza and nasal congestion. Fever, dyspnea, cough, malaise. Retraction nasal flaring, wheezing/rhonchi, tachypnea. Bacterial: No symptoms, differentiating from viral pneumonia, but in children it presents with fever and distress, headaches, malaise, abdominal pain, productive cough with sputum, chest pain during inspiration. Crackles, decreased breath sounds, increased fremitus and dullness to percusssion

You are the RT in a busy urban trauma center in Phoenix, Arizona. It is the middle of summer with temperatures reaching over 100 degrees daily. A 7-year-old was brought into the emergency department by her mother following a day spent at the babysitter's house. The mother states that she brought the patient in because the patient's heart was racing. The mother stated, "the babysitter said she was playing outside all day and seemed fine." What possible type of shock could be the cause for the 7-year-old's fast heart rate? How would it be treated?

What could be a possible problem that should be explored as a cause for the 7-year-old's fast heart rate? Hypovolemic shock is most common worldwide among infants and children, most often resulting from severe dehydration. Healthy children often have intact compensatory mechanisms, which allow them to tolerate acute volume of losses of 10% to 15% of their circulatory blood volume. Early signs of compensated hypovolemic shock include tachycardia, decreased pulse pressure, and peripheral vasoconstriction, with often a normal systemic arterial blood pressure. How would it be treated? With timely and aggressive volume resuscitation, this shock state can readily be reversed.

A 3.7-kg newborn female is delivered via an elective cesarean section at 41 weeks of gestation. Apgar scores were 7 and 8 at 1 and 5 minutes, respectively. The infant's temperature is 96.4° F (35.8° C), respiratory rate is 92 breaths/min, and heart rate is 143 beats/min. She has subcostal and intercostal retractions. The remainder of the examination is normal. The chest radiograph is shown in Figure 22-5 in the text. Over the next 6 hours she improves and no longer requires oxygen.

What is the diagnosis? Answer: Respiratory distress in a full-term neonate is most probably transient tachypnea of the neoborn (TTN) but we have to exclude other causes of neonatal respiratory distress. TTN is a clinical diagnosis. And because it is similar in its initial presentation to conditions such as RDS, sepsis/pneumonia and PPHN, TTN is often a diagnosis of exclusion; unless symptoms are mild and rapidly improving, alternative diagnosis should be considered. The parents are worried about her prognosis. What would you tell them? Answer: Transient tachypnea of the newborn is a relatively benign, typically self-limited disease that occurs in approximately 5 of 1000 infants delivered between 37 and 42 weeks of gestation. It is most common after elective cesarean section delivery without labor. The condition is self-limited. The distress, hypoxemia, and mild respiratory acidosis usually resolve within 48 hours. Complications are rare, though air leaks may occur, particularly if the baby has required support with positive pressure ventilation.

A 14-year-old girl presents to the emergency room complaining of sore throat, fever, and dysphagia. She has no prior health issues and no known sick contact. She says she had been well the day before and noticed her symptoms on awakening in the morning. Physical findings include a mild stridor on auscultation over both apical lung fields and over the trachea. Inspection of the retropharynx is complicated by the patient not being able to open her mouth, but you can see that the uvula is being displaced to the left. She also has problems rotating her head to the left.

What is the most likely diagnosis and what would be your next step in diagnosis? What is the treatment? Answer: Because of her age and classic findings, peritonsillar abscess is suspected. Patients commonly complain about trismus (difficulty opening their mouth), sore throat, torticollis, and muffled or hoarse voice. The diagnosis is made clinically and by culture; if in doubt, frontal anteroposterior and lateral radiographs of the head and neck can aid in the diagnosis. The most likely causative organisms are Streptococcus pyogenes (group A streptococcus) or Staphylococcus aureus.

A 13-month-old former 24-week-gestation premature infant with resolving BPD is brought to his pediatrician with a 2-day history of decreased appetite, runny nose, and increased cough. It is February. His O2 saturation, vitals, and exam are unremarkable and the decision is made to discharge him home with close follow-up. Two days later his O2 requirement is up to 1 L/min O2 via nasal cannula (from 0.25 L/min O2 via nasal cannula), and he exhibits increased respiratory distress. O2 saturation is decreased to 80% and he is afebrile. He is admitted to the hospital with decreased PO intake and respiratory distress. A rapid RSV test is positive, and his chest X-ray shows infiltrates in the right middle lobe and the left upper lobe.

What is your diagnosis and treatment? Answer: RSV infections demonstrate the difficulty of distinguishing between bacterial and viral pneumonias. In the case of a child with underlying lung disease, such as BPD, this may lead to a more conservative and widespread use of antibiotics. Hypoxemia and hypercarbia are complications of RSV pneumonia and may mandate supplemental oxygen for an extended period. Supportive care is aimed at monitoring the severity with pulse oximetry. Patients may experience progressive hypoxemia and respiratory failure, necessitating intubation and mechanical ventilation. There may be further progression to advanced respiratory failure, in spite of maximal ventilatory support. Those patients may require extracorporeal membrane oxygenation (ECMO).

A 2-year-old girl arrives in the emergency room intubated with a 4.0 ETT by EMS. The mother states the toddler had been ill for several days with a runny nose, fever, and a cough. The night before the mother had noted that the girl was breathing "funny" and had a barking cough. This morning she refused to drink, had increased difficulty breathing, and was very irritable. She has had multiple episodes of vomiting with coughing, but no diarrhea. After consulting her pediatrician by phone, she had been advised to call an ambulance and have the child transported to the hospital. EMS reports to have found the toddler in respiratory distress and in an altered mental state. Marked stridor was audible and the oxygen saturation was measured at 58%. The infant was sedated and paralyzed; the intubation with the 4.0 ETT was extremely difficult and required multiple attempts.

What is your differential diagnosis? Answer: Laryngotracheobronchitis. Patient treatment is largely supportive. A lateral neck radiograph, sometimes obtained to help differentiate the disease from epiglottitis, demonstrates a large retropharyngeal air shadow without epiglottic swelling. The anteroposterior chest radiograph reveals the classic "steeple sign," a sharply sloped, wedge-shaped, linear narrowing of the trachea. What treatment should you recommend? Answer: Treatment of mild cases of LTB is largely supportive—ensuring temperature control, adequate hydration, and humidification of inspired air. Techniques to cool the airway have traditionally used humidified air with water particles large enough to "rain out" onto the upper airway and tracheal mucosa. Nebulized racemic epinephrine is used to induce vasoconstriction of the upper airway. This child is a severe case in which dexamethasone will certainly be given. Administration of oral dexamethasone at 0.6 mg/kg has been recommended as the least expensive and least invasive means by which to lower hospitalization rates. The size of the ETT is a little small but certainly manageable. What complications should you expect? Answer: Avoiding ventilator-induced lung injury will be paramount because these children tend to have normal lung function. To avoid traumatizing the inflamed subglottic tissue, the ETT should be at least 1 mm smaller in diameter than that estimated for the child's age. As with epiglottitis, dramatic improvement in respiratory distress is expected after intubation. Attempts at extubation can be made if an air leak develops around the ETT at pressures under 20 to 30 cm H2O. The child is closely monitored in the 4 to 12 hours after extubation for the return of stridor.

A 3½-year-old boy is admitted to the intensive care unit (ICU) after heart surgery. He was on cardiopulmonary bypass for 190 minutes and the operation went well. In the ICU he is sedated and ventilated. A chest radiograph and cultures are obtained on postoperative day 1 for fever. The chest radiograph shows consolidation of the left lower lobe, and it remains the same over the next days. All cultures are negative, and he is successfully extubated on postoperative day 4. The chest radiographs remain unchanged, and the decision for bronchoscopy is made. Before the bronchoscopy the plan is to reintubate the child. He is paralyzed, and his baseline oxygen saturation remains at 75% to 79% under bag-mask ventilation. An ETT is placed under good visualization of the vocal cords, but his oxygen saturations fall to 60% to 65% with minimal chest rise and increased resistance to bagging. He is extubated, and it is not possible to bag-mask ventilate him. His oxygen saturations continue to drop, and after a second intubation attempt with good visualization of the vocal cords, he goes into cardiac arrest.

What is your differential diagnosis? Answer: Atalectasis and bronchiectasis What are your actions? Answer: Atelectasis is collapsed lung parenchyma and is best compared to a wet sponge that fails to reinflate after being compressed. Many processes can cause atelectasis. Internal or parenchymal disorders that are characterized by an inadequate tidal volume, loss of lung compliance (e.g., acute respiratory distress syndrome), airway obstruction (e.g., mucus plugging), and increased elastance of lung tissue can all result in atelectasis. Postoperative patients are at particular risk of atelectasis because of an ineffective cough, impaired mucus transport, and the effect of anesthesia. Tracheobronchial suctioning has also been related to atelectasis in children and is believed to result from the negative pressure that the airway is exposed to during the suctioning process. Resuscitation efforts should immediately be started. Bronchiectasis is defined as irreversible dilation of the bronchial tree. Typically, the segmental and subsegmental bronchi become irregularly shaped and dilated, leading to a loss of the typical funnel configuration that allows smooth central flow of secretions. Additionally, ciliary activity in the area of the dilation is inadequate and further contributes to the difficulty in mobilizing secretions. The secretions become infected as they pool. The lower lobes, particularly the left lower lobe, are most often involved.

A 3.5-kg male infant is vaginally delivered with amniotic fluid stained with thick meconium. He is initially limp and without strong respiratory effort but has a heart rate greater than 100 bpm. He responds to appropriate resuscitation with improvement in respiratory effort but remains cyanotic and tachypneic. Apgar scores are 4 and 6 at 1 and 5 minutes, respectively. After admission to the NICU, the infant's temperature is 98.4° F (36.9° C), heart rate is 173 beats/min, respiratory rate is 110 breaths/min, and mean blood pressure is 61 mm Hg. He is barrel chested and has retractions with poor-to-fair air entry. Coarse crepitations are audible bilaterally. The chest radiograph is shown in Figure 22-8 in the text.

What is your provisional diagnosis? Answer: With an APGAR scores and meconium-stained amniotic fluid, meconium aspiration syndrome is a provisional diagnosis. How would you resuscitate this neonate? The American Academy of Pediatrics Neonatal Resuscitation Program Steering Committee and the American Heart Association have updated guidelines for management of the baby exposed to meconium in the 2015 Neonatal Resuscitation Program. One of the significant changes in the current guidelines are removal of recommendations to suction the trachea of non-vigorous infants born through MSAF. Performing elective endotracheal suctioning of meconium does not offer benefit in preventing MAS based on a lack of evidence demonstrating benefit and aiming to avoid harm. The AAP and AHA no longer recommend routine immediate endotracheal intubation and suctioning for nonvigorous infants. The care for these infants is guided by the same principles as outlined in NRP, in which intubation is indicated for inadequate respiratory effort (apnea, gasping, or poor oxygenation) or bradycardia despite bag mask ventilation, or when chest compressions are required. How would you monitor and initially manage respiratory distress in this neonate? The goal is to maintain acceptable systemic oxygenation. Generally, this consists of sustaining peripheral oxygen saturation between 95% and 99% or Pao2 between 60 and 80 mm Hg. Oxygen is also a pulmonary vasodilator, therefor hypoxia should be avoided. CPAP may be considered in infants who require FiO22 > 0.4.

Effects of MAS on the neonate?

When aspirated, it can cause a release of cytokines, serious airway obstruction, air trapping, and enhanced growth of bacteria. Enzymes of meconium can break down certain surfactant components. Depending on the extent of stress or hypoxia, the infant may be depressed at birth and then quickly develop cyanosis and respiratory distress, including gasping, respirations, grunting, retractions, nasal flaring, and tachypnea.

*Meconium Aspiration* incidence, cause, and pathophysiology

When meconium is aspirated in the lung, it may cause a release of cytokines, airway obstruction, air trapping, and enhanced growth of bacteria. -Sign of intrauterine stress or hypoxia.