1. NEONATAL RESPIRATORY DISORDERS
DR. MAHMOUD MOHAMED OSMAN
MBBCh, MSc (Pedia), MRCPCH (UK), FRCP (Edinburgh)
Consultant Pediatrician & Neonatologist
Al Yammamah Hospital , MOH

2. OBJECTIVES: Respiratory distress (General)
Respiratory distress syndrome
Transient tachypnea of the newborn
Meconium aspiration syndrome
Pulmonary air leaks
Neonatal apnea

3. INTRODUCTION

4. 1) Respiratory Distress:
Respiratory distress is a general term used to describe respiratory symptoms and is not synonymous with respiratory distress syndrome (RDS).
Signs of respiratory distress include:
Tachypnea – a respiratory rate greater than 60/min.
Expiratory grunt – breathing against a closed glottis.
Chest retraction or recession.
Flaring of the nostrils.
Cyanosis or low arterial oxygen saturation in room air.

5. 2) Common causes of respiratory distress:
A - Primary Respiratory Causes:
Transient tachypnea of the newborn
RDS due to surfactant deficiency [Preterms]
Aspiration syndromes {meconium, milk, blood}
Pulmonary air leaks {Pneumothorax; pneumomediastinum}
Pneumonia
Pulmonary hypoplasia {with oligohydramnios}
Pulmonary haemorrhage
Chronic neonatal lung disease {BPD}

6. B- Secondary to extrapulmonary pathology: Congenital heart diseases.
Birth asphyxia.
Infections (Sepsis).
Surgical conditions:
Choanal atresia.
Pierre robin sequence.
Diaphragmatic hernia.
Lobar emphysema.
Tracheo-oesophageal fistula.
Persistence of fetal circulation (PPHN) .
Anaemia , Polycythaemia.
Metabolic diseases.

7. 3. Diagnosis of Respiratory Distress:
A full Perinatal history includes
Gestational age
Polyhydramnios, or oligohydramnios
Anomalies on ultrasound
Risk factors for sepsis
The passage of meconium
Poor condition at birth
Duration of amniotic membrane rupture.
Physical examination includes
Observation of vital signs and auscultation of the lungs for symmetry of air entry, and heart sounds.
Appropriate investigations

8. Investigations for respiratory distress:
Chest radiograph.
Bacteriological cultures on blood, urine and cerebrospinal fluid (CSF).
Viral cultures and rapid-yield immunodiagnostic tests.
Haematocrit and full blood count.
Chest transillumination if pneumothorax is suspected.
Passage of nasogastric catheters if choanal or oesophageal atresias are suspected.
Hyperoxia test to differentiate between cardiac and respiratory disease.
Echocardiography.

9. 4. Treatment of respiratory distress
Supportive care
The supportive care of the infant with respiratory distress is similar regardless of etiology.
Infants with respiratory distress require:
Frequent or continuous observations of respiratory and heart rates, temperature, blood pressure and signs of respiratory distress.
Accurate fluid balance charts are essential.
Adequate temperature control
Adequate nutrition is essential part of respiratory care

10. Oxygen
Oxygen is a useful and life-saving therapeutic agent, but is also potentially dangerous, particularly in the preterm baby, as it may damage the eyes (retinopathy of prematurity), or the lungs (bronchopulmonary dysplasia).
Oxygen should be warmed to 34–37°C and humidified.
Fluids
In mild respiratory distress nasogastric feeding may be adequate.
In moderate to severe respiratory distress; babies should not be enterally fed.
Intravenous fluids will be required. Usually a 10% dextrose and electrolytes or total parenteral nutrition. .

11. 4. Blood gases and acid–base status
Assessment of the arterial acid–base status, with samples from an intra-arterial catheter or capillary blood gases.
Continuous transcutaneous monitoring of PO2 and PCO2 decreases blood sampling and enables rapid detection of fluctuations in clinical status.
If respiratory acidosis is severe (pH <7.20 with PCO2 >60 mmHg) assisted ventilation may be necessary.
For a severe metabolic acidosis (base deficit > −8), an infusion of sodium bicarbonate may be indicated.
But one should always try to treat the underlying cause first !!!!.

13. 5. Artificial respiratory support
In more severe cases artificial respiratory support may be necessary.
This may be in the form of noninvasive respiratory support such as:
Continuous positive airway pressure (CPAP)
Bilevel positive airway pressure (BiPAP) or
Non-invasive positive-pressure ventilation (NIPPV)
In a proportion of cases, such treatment may fail and switch to invasive mechanical ventilation becomes a must.

14. Indications for mechanical ventilation
• Failure to initiate or establish spontaneous breathing.
• Worsening apneas and bradycardias.
• Major respiratory or cardiac collapse.
• Surfactant administration.
• Need to maintain airway patency.
• Impaired pulmonary gas exchange.

15. 6. Treatment of the Etiological Cause:
Medical or surgical treatment of the etiological cause is the cornerstone in management of the neonatal respiratory diseases.

16. 1. Respiratory Distress Syndrome

17. Pathophysiology:
The primary cause of respiratory distress syndrome, also known as (hyaline membrane disease (HMD)), is inadequate production of surfactant due to prematurity.
The manifestations of the disease are caused by the diffuse alveolar atelectasis, edema, and cell injury.
Subsequently, serum proteins that inhibit surfactant function leak into the alveoli.

18. Interdependent relationship of factors involved in pathology of respiratory distress syndrome.

19. The lung in respiratory distress syndrome of the neonate
The lung in respiratory distress syndrome of the neonate. The alveoli are atelectatic, and a dilated alveolar duct is lined by a fibrin-rich hyaline membrane.

20. Advances made in the management of RDS include :
Prenatal diagnosis to identify infants at risk.
Antenatal administration of glucocorticoids.
Improvements in perinatal and neonatal care.
Surfactant replacement therapy.
As a result:
The mortality from RDS has decreased.
Survival of increasing numbers of extremely immature infants has provided new challenges.
But also, RDS remains an important contributing cause of neonatal mortality and morbidity.

21. I. DIAGNOSIS: A. Perinatal risk factors
1. Factors that affect lung development at birth:
Prematurity, maternal diabetes, and genetic factors (white race, history of RDS in siblings, male sex).
Thoracic malformations that cause lung hypoplasia, (such as diaphragmatic hernia).
Genetic disorders of surfactant production and metabolism (such as surfactant protein B or C deficiency cause a severe RDS like picture, often in term infants).
2. Factors acutely impair surfactant function:
Perinatal asphyxia in premature infants.
Cesarean section before labor starts.

22. B. Postnatal diagnosis.
A premature infant with RDS has clinical signs shortly after birth.
These include tachypnea, retractions, nasal flaring, grunting, and cyanosis.
The classic radiographic appearance is of low- volume lungs with a characteristic diffuse reticulogranular pattern ‘ground glass’ appearance, and air bronchograms.

23. II. MANAGEMENT: General lines of manegment
Prevent hypoxemia and acidosis.
Optimize fluid management.
Reduce metabolic demands.
Prevent atelectasis and pulmonary edema.
Minimize lung injury caused by oxygen, or mechanical ventilation.
Specific lines of manegment
Surfactant replacement therapy
Continuous positive airway pressure
Mechanical ventilation
Supportive therapy

24. III. Antenatal corticosteroid therapy (Prophylaxes):
Should be given to pregnant women 24 to 34 weeks‘ gestation with intact membranes or with (PROM) without chorioamnionitis, who are at high risk for delivery within the next 7 days.
It induces sufactant production and accelerates maturation of the lungs and other fetal tissues.
It results in marked reduction of :
RDS,
Intraventricular hemorrhage (IVH),
Necrotizing enterocolitis, and
Perinatal mortality.
Drugs used are: betamethasone or dexamethasone .

25. III. COMPLICATIONS: Pneumothorax, and other air leaks
Patent ductus arteriosus (PDA).
Subglottic stenosis (causing stridor).
Chronic lung disease (CLD).
Necrotising enterocolitis (NEC).
Intraventricular-periventricular haemorrhage.
Periventricular leukomalacia (PVL).
Retinopathy of prematurity (ROP).

26. 2. TRANSIENT TACHYPNOEA OF THE NEWBORN

27. I. DEFINITION.
Transient tachypnea of the newborn (TTN), known as wet lung, is a relatively mild, self-limited disorder most commonly affecting infants who are born at or near term.
Transient tachypnea of the newborn occurs in 1–2% of all newborn infants and is due to respiratory mal-adaptation at birth causing retention of fluids in the lungs.
Tachypnea is generally the outstanding feature.
TTN is usually benign and self-limiting, with symptoms rarely persisting beyond 48 hs.

28. II. PATHOPHYSIOLOGY.
Disruption or delay in clearance of fetal lung liquid from a number of conditions results in the transient pulmonary edema that characterizes TTN.
Retained fluid accumulates in the peribronchiolar lymphatics and bronchovascular spaces, causing compression and bronchiolar collapse with areas of air trapping and hyperinflation.
These changes result in a net decrease in lung compliance accounting for the clinical manifestations of the condition.

29. Characteristic features of retained pulmonary fluid with airspace filling and fluid in the horizontal fissure.

30. III. RISK FACTORS.
Premature birth, precipitous birth, and operative birth without labor, associated with an increased risk of TTN.
Delayed cord clamping or cord milking, promoting placental-fetal transfusion, leads to an elevation in the central venous pressure.
Congenital disrupting clearance of fluid by the thoracic duct or pulmonary lymphatics.
Additional risk factors include:
Birth to an asthmatic mother.
Excessive maternal sedation.
Administration of large amounts of IVF to the mother.
Male gender, macrosomia and multiple gestations.

31. lV. DIFFERENTIAL DIAGNOSIS AND EVALUATION.
Diagnosis of TTN requires the exclusion of other potential etiologies for respiratory distress presenting in the first 6 hous of age.
The differential diagnosis includes:
Pneumonia - sepsis,
Cyanotic congenital heart disease,
Hyaline membrane disease (HMD),
Pulmonary hypertension,
Meconium aspiration,
Hypoxic-ischemic encephalopathy (HIE),
Polycythemia.

32. V. INVESTIGATIONS & MANAGEMENT.
A full sepsis evaluation, including complete blood count and appropriate cultures (pneumonia or sepsis) should be done.
If risk factors or laboratory data suggest sepsis, or if respiratory distress does not improve within 4 hours, initiate broad-spectrum antibiotics.
TTN does not usually require respiratory support, other than extra inspired oxygen.
Regular blood-gas measurements .
In more severe cases CPAP may aid resolution
Diuretic therapy has no significant effect. .

33. If the condition still deteriorated:
The diagnosis should be reconsidered.
Complications such as pulmonary hypertension or pneumothorax may have developed.

34. 3. MECONIUM ASPIRATION SYNDROME

35. I. BACKGROUND
A. Cause.
Acute or chronic hypoxia and/or infection can result in the passage of meconium.
In this setting, gasping by the fetus or newly born infant can cause aspiration of amniotic fluid contaminated by meconium.
Meconium aspiration before or during birth can obstruct airways, interfere with gas exchange, and cause severe respiratory distress.

36. B. Incidence.
Meconium-stained amniotic fluid (MSAF) complicates delivery in approximately 8% to 15% of live births.
The incidence of MSAF in preterm infants is very low.
Most meconium-stained infants are post-mature and small for gestetianal age (SGA).
Approximately 5% of neonates born through MSAF develop meconium aspiration syndrome (MAS).
Approximately 50% of meconium aspiration syndrome infants require mechanical ventilation.

37. II. Pathogenesis:
Meconium causes a number of anatomical and physiological problems that make lung function worse:
Plugging of the airways, with consequent atelectasis.
Meconium causes a ‘ball-valve’ obstruction with hyperinflation of the lungs and a high risk of pulmonary air leaks.
Meconium irritations the airways, causing a chemical pneumonitis.
Meconium impairs surfactant production and function.
Possible secondary bacterial infection.

38. In a proportion of babies with severe MAS, there is development of marked persistent pulmonary hypertension (PPHN), with right-to-left shunt at PFO& PDA.

39. Meconium Aspiration Syndrome (MAS)

40. Severe MAS & Rt sided pneumothorax before and after drainage.

41. III. PREVENTION OF MAS A. Prevention of passage of meconium in utero.
Mothers at risk for placental insufficiency include:
Those with preeclampsia or increased blood pressure.
Chronic respiratory or cardiovascular disease.
Poor uterine growth.
Post-term pregnancy.
Heavy smokers.
These women should be carefully monitored during pregnancy.
In pregnancies past the due date, induction as early as 41 weeks may help prevent MAS by avoiding passage of meconium.

42. IV. LABOUR ROOM MANAGEMENT:
During labor the fetal heart rate should be monitored, with fetal scalp blood samples obtained for pH determination.
If the infant appears vigorous, routine care should be provided, regardless of the meconium.
If respiratory distress develops or the infant becomes depressed, the trachea should be intubated, and intratracheal suctioning performed.
In questionable cases, it is safer to intubate and do suction, as MAS can occur in infants delivered through thinly stained amniotic fluid.

43. V. NICU MANAGEMENT OF MAS: A. Observation.
Infants who are depressed at birth should be closely observed.
A chest radiograph may help determine those infants who are most likely to develop respiratory distress.
A number of asymptomatic infants will have an abnormal-appearing chest.
The classic findings are diffuse, asymmetric patchy infiltrates, areas of consolidation, and hyperinflation.

44. B. Routine care.
1. The infant should be maintained in a neutral thermal environment.
2. Monitor blood glucose, calcium, and electrolytes.
3. Severely depressed infants may have metabolic acidosis that to be corrected.
4. Fluids should be restricted to prevent cerebral and pulmonary edema.
5. Circulatory support with normal saline, dopamine, or packed red blood cells.
(hemoglobin >15 g ; hematocrit > 40%).
6. Renal function should be continuously monitored .

45. C. Oxygen therapy.
- Monitoring blood gases and pH aids assessment of the severity and avoids hypoxemia .
- Hypoxic insults may result in pulmonary vasoconstriction and contribute to the development of PPHN.
- Management of hypoxemia by increasing the inspired oxygen.
D. Assisted ventilation Mechanical ventilation is indicated for excessive co2 retention (Paco2 >60 mm Hg) or for persistent hypoxemia (Pao2<50 mm Hg).
Continuous positive airway pressure (CPAP).
Conventional mechanical ventilation.
High-frequency ventilation with oscillatory ventilators.
The use of sedation and muscle relaxation.

46. E. Medications. 1. Antibiotics.
Differentiating between bacterial pneumonia and meconium aspiration by clinical course and chest x-ray may be difficult.
The use of broad-spectrum antibiotics (Ampicillin and gentamicin) is usually indicated.
Blood cultures should be obtained to identify bacterial disease.
2. Surfactant.
Surfactant treatment of MAS may improve oxygenation and reduce pulmonary complications and the need for (ECMO).
3. Corticosteroids.
We do not recommend the use of corticosteroids in MAS. .

47. F. Complications 2. PPHN 3. Pulmonary sequelae.
1. Air leak.
Peumothorax or pneumomediastium occurs in approximately % to 33% of patients with MAS, more frequently with mechanical ventilation.
2. PPHN
Is associated with MAS in approximately one third of cases.
Echocardiography should be performed to ascertain the degree of PPHN; and to exclude congenital heart disease.
In severely ill infants with MAS and PPHN, inhaled nitric oxide (iNO) reduces the need for ECMO.
3. Pulmonary sequelae.
Higher incidence of pneumonia.
Approximately 5% of survivors require oxygen at 1 month.
Some have abnormal pulmonary functions (increased functional residual capacity, airway reactivity)

48. 4. PULMONARY AIR LEAKS

49. A. Incidence and risk factors.
Risk factors for air leak in premature infants: Include respiratory distress syndrome (RDS), mechanical ventilation, sepsis, and pneumonia Surfactant therapy for RDS has markedly decreased the incidence of pneumothorax.
Risk factors in term infants:
- Aspiration of meconium, blood, or amniotic fluid; pneumonia; congenital malformations; and mechanical ventilation.

50. B. Pathogenesis. Air leak syndromes arise through a common mechanism.
Transpulmonary pressures that exceed the strength of the terminal airways and alveoli can damage the respiratory epithelium.
The air enters the interstitium, causing pulmonary interstitial emphysema.
Then dissection of air toward the visceral pleura and/or the hilum through the peribronchial and perivascular spaces.
Rupture of the pleural surface allows the adventitial air to decompress:
Into the pleural space Pneumothorax.
Into the mediastinum Pneumomediastinum
Into the pericardium Pneumopericardium
Into the fascial and neck skin Subcutaneous emphysema
Into the retroperitoneum, peritoneum Pneumoperitoneum
Into the scrotum or labial folds Pneumoscrotum
In rare circumstances, air can enter the pulmonary veins and result in an Air embolism.

51. B, Pneumothorax (tension) has compressed a stiff lung, depressed the right side of the diaphragm
A, Pulmonary interstitial emphysema.

52. C, Pneumopericardium Radiograph shows a broad halo of air around the heart. Pulmonary interstitial emphysema affects the right lung. The diagram indicates the path of air from the lung interstitium to the pericardium

53. C . TYPES OF AIR LEAKS

54. A. Pulmonary interstitial emphysema (PIE)
Occurs most often in mechanically ventilated, extremely preterm infants with RDS or sepsis.
Interstitial air can dissect toward the hilum and the pleural surface through the connective tissue surrounding the peribronchial, lymphatics and pulmonary vessels.
This can compromise lymphatic drainage and pulmonary blood flow.
PIE alters pulmonary mechanics by decreasing compliance, increasing residual volume and dead space, and enhancing ventilation/perfusion mismatch.
Rupture of interstitial air into the pleural space and mediastinum can result in pneumothorax and pneumomediastinum, respectively.

55. 1. Diagnosis PIE frequently develops in the first 48 hours of life.
PIE may be accompanied by hypotension, bradycardia, hypercapnia, hypoxia, and acidosis.
PIE has two radiographic patterns; cyst like and linear:
Linear lucencies radiate from the lung hilum.
Small cyst-like blebs
Occasionally, large cyst-like blebs give the appearance of a pneumothorax.

56. Chest radiograph showing extensive PIE
Chest radiograph showing extensive PIE Note the overinflated chest with flattened diaphragm.

57. A. Severe bilateral PIE, with gross cardiac compression
A. Severe bilateral PIE, with gross cardiac compression. A chest drain is in situ in the right hemithorax. B. Postmortum PIE Right lung

58. 2. Treatment. 3. Complications.
If possible, try to decrease mean airway pressure.
High-frequency oscillatory ventilation in infants with PIE to avoid large swings in lung volume.
Unilateral PIE may improve if the infant is positioned with the affected lung dependent.
Endotracheal suctioning and manual positive pressure ventilation should be minimized.
Selective bronchial intubation or occlusion or, rarely, surgical resection.
3. Complications.
PIE may precede more severe complications such as pneumothorax, pneumopericardium, or an air embolus.

59. B. Pneumothorax.
Spontaneous pneumothorax occurs rarely in healthy neonates. One in ten of these infants is symptomatic
Pneumothorax is more common in newborns treated with mechanical ventilation for underlying lung disease.
Clinical signs of pneumothorax range from insidious changes in vital signs to the complete cardiovascular collapse that accompanies a tension pneumothorax.
A pneumothorax must be considered in mechanically ventilated infants who develop unexplained deterioration.

60. 1. Diagnosis: a. Physical examination: b. Arterial blood gases.
Nonspecific and demonstrate a decreased Po2 and increased Pco2 (decreased pH).
c. Chest radiograph.
S hows a hyperlucent hemithorax, a separation of the visceral from the parietal pleura, flattening of the diaphragm, and mediastinal shift
d. Transillumination.
A high-intensity fiber optic light source may demonstrate a pneumothorax.
e. Needle aspiration.
In a rapidly deteriorating clinical situation, thoracentesis may confirm the diagnosis and be therapeutic.

61. Neonates With Pneumothoraces

62. Diagnosis of Pneumothorax through transillumination

63. 2. Treatment:
Conservative therapy: Close observation may be adequate for infants who have no underlying lung disease or complicating therapy , are in no severe respiratory distress, and have no continuous air leak.
-The extrapulmonary air will usually resolve in 24 to 48 hours
Needle aspiration: Thoracentesis with a “butterfly” needle or intravenous catheter can be used to treat a symptomatic pneumothorax. { May be life-saving }
- Needle aspiration may be curative in infants not receiving mechanical ventilation .
Chest tube drainage: Chest tube drainage is generally needed to evacuate pneumothoraces in infants receiving mechanical ventilation.
- Frequently, these air leaks are continuous and will result in severe hemodynamic compromise if left untreated.

64. Intraventricular hemorrhage may result.
4. High-frequency oscillation ventilation (HFOV): Persistent pneumothorax refractory to routine measures may improve with high-frequency oscillation ventilation.
5. Extracorporeal membrane oxygenation (ECMO): Some infants require extracorporeal membrane oxygenation (ECMO)
3. Complications
Profound ventilatory and circulatory compromise can occur and, if untreated, result in death.
Intraventricular hemorrhage may result.
Inappropriate antidiuretic hormone secretion may occur.
Development of other air leaks.

65. C. Pneumomediastinum.
Mediastinal air develops when interstitial air dissects into the mediastinum
When direct trauma occurs to the airways or the posterior pharynx.
Pneumomediastinum may occur with other air leaks.
1. Diagnosis
Physical examination. Heart sounds may appear distant.
Chest radiograph.
Air collections are central and usually elevate or surround the thymus “spinnaker sail” sign.
Pneumomediastinum is best seen on a lateral view.

66. 2. Treatment.
Pneumomediastinum is of little clinical importance, and specific drainage procedures are usually unnecessary.
Rarely, if the air is under tension, cardiorespiratory compromise may develop, and this situation may require mediastinostomy drainage.
If the infant is mechanically ventilated, reduce mean airway pressure if possible.

67. A
Newborn with mild respiratory distress; had pneumomediastinum elevating the thymus (Thymic sail sign).

69. D. Pneumopericardium.
Pneumopericardium is the least common form of air leak in newborns but the most common cause of cardiac tamponade.
Asymptomatic pneumopericardium is occasionally detected as an incidental finding on a chest radiograph.
Most cases occur in preterm infants with RDS treated with mechanical ventilation, preceded by PIE and pneumomediastinum.
The mortality rate for critically ill infants who develop pneumopericardium is 70% to 80%.

70. 1. Diagnosis. Chest radiograph. Transillumination.
Physical examination.
Infants may initially have tachycardia and decreased pulse pressure, but hypotension, bradycardia, and cyanosis may ensue rapidly.
Auscultation reveals muffled or distant heart sounds.
Chest radiograph.
Anteroposterior views show air surrounding the heart.
Air under the inferior surface of the heart is diagnostic.
Transillumination.
A high-intensity fiberoptic light source may illuminate the substernal region.
Flickering of the light with the heart rate may help differentiate pneumopericardium from pneumomediastinum.
Electrocardiogram (ECG).
Decreased voltages, manifest by a shrinking QRS complex, are consistent with pneumopericardium.

71. Pneumopericardium with air completely surrounding the heart, demarcating the pericardial sac.

72. 2. Treatment A. Conservative management.
- Asymptomatic infants not receiving positive pressure ventilation can be managed expectantly.
- Vital signs are closely monitored (especially pulse pressure).
- Frequent chest radiographs are obtained.
B. Needle aspiration.
- Cardiac tamponade is a life-threatening event that requires immediate pericardiocentesis.
C. Continuous pericardial drainage.
- Pneumopericardium often progresses to cardiac tamponade and may recur.
- Pericardial tube may be needed for continuous drainage.

73. 3. Complications.
Ventilated infants who have pneumopericardium drained by needle aspiration frequently (80%) have a recurrence.
Recurrent pneumopericardium can occur days after apparent resolution of the initial event.
Cardiac tamponade.

74. E. Other types of air leaks:
1. Pneumoperitoneum.
Intraperitoneal air may result from extrapulmonary air that decompresses into the abdominal cavity.
Usually the pneumoperitoneum is of little clinical importance, but it must be differentiated from intraperitoneal air resulting from a perforated viscus.
Rarely, pneumoperitoneum can impair diaphragmatic excursion and compromise ventilation In these cases, continuous drainage may be necessary.

75. Pneumoperitoneum developing secondary to pulmonary interstitial emphysema and pneumothoraces.

76. 2. Subcutaneous emphysema.
Subcutaneous air can be detected by palpation of crepitus in the face, neck, or supraclavicular region.
Large collections of air in the neck, although usually of no clinical significance, can partially occlude or obstruct the compressible, cartilaginous trachea of the premature infant.

77. Subcutaneous emphysema due to
tension pneumothorax

78. 3. Systemic air embolism.
An air embolism is a rare but usually fatal complication of pulmonary air leak.
Air may enter the vasculature either by disruption of the pulmonary venous system or by inadvertent injection through an intravascular catheter.
The presence of air bubbles in blood withdrawn from an umbilical artery catheter can be diagnostic.

79. 5. NEONATAL APNEA

80. 1. INTRODUCTION:
Apnea is defined as cessation of breathing that lasts for at least 20 seconds and is accompanied by bradycardia, oxygen desaturation, or cyanosis.
Apnea is common in preterm neonates and is a significant clinical problem. It is manifested by an unstable respiratory rhythm, reflecting the immaturity of the respiratory control system.
Apnea can also be secondary to other pathological conditions, which need to be excluded before the diagnosis of apnea of prematurity is assumed.
In contrast, periodic breathing is a benign condition and does not merit any treatment.

81. 2. TYPES OF APNEA: A. Central apnea. B. Obstructive apnea.
Total cessation of inspiratory effort with no evidence of obstruction.
B. Obstructive apnea.
Infant tries to breathe against an obstructed airway resulting in chest wall motion without air flow throughout the apneic episode.
C. Mixed apnea.
Consists of obstructed respiratory efforts usually followed by central apnea. Purely obstructive apnea is probably uncommon.
D. Periodic breathing.
Periodic breathing consists of breathing for 10 to 15 seconds followed by apnea for 5 or10 seconds, without change in heart rate or skin color.
It is due to an imbalance between the effect of peripheral and central chemoreceptors on ventilatory drive.
The prognosis is good.

82. 3. Incidence.
The incidence of apnea and periodic breathing in the term infant has not been adequately determined.
Periodic breathing is common in preterm infants It is more frequent during active sleep.
More than 50% of infants weighing <1500 gm, and % of infants weighing <1000 gm have apnea.
Mixed apnea is the most common type (50%), followed by central (40%), and then obstructive (10%).

83. 4. Risk factors A- Physiologic immaturity of the respiratory center:
This condition is usually present after 1–2 days of life, and is often referred to as apnea of prematurity (AOP).
B- Secondary causes:
1- Neurologic.
Birth trauma, meningitis, intracranial hemorrhage, seizures, perinatal asphyxia, congenital myopathies or neuropathies.
Placental transfer of narcotics, magnesium sulfate, or general anesthetics.
2- Pulmonary.
Surfactant deficiency, pneumonia, pulmonary hemorrhage, obstructive airway lesions, pneumothorax, hypoxemia.

84. 3. Cardiac.
Cyanotic congenital heart disease, hyper- or hypotension, congestive heart failure, patent ductus arteriosis, increased vagal tone, and prostaglandin therapy.
4. Hypothermia or hyperthermia.
5. Metabolic.
Acidosis, hypoglycemia, hypocalcemia, and hypo- or hypernatremia.
6. Hematologic. Anemia.
7. Sepsis.
8. Gastrointestinal.
GERD and necrotizing enterocolitis (NEC).

85. Specific Contributory Causes of Apnea.

86. 5. Clinical manifestations.
It is difficult to separate clinical manifestations of apnea from consequences of apnea.
Symptoms and signs depend on the duration and frequency of apnea and most are related to hypoxia.
Other clinical manifestations depend on the etiology of apnea such as:
Temperature instability,
Poor feeding; feeding intolerance,
Jitteriness,, irritability, seizures.
Lethargy, hypotonia,
Central nervous system depression,
Desaturation, tachycardia, bradycardia.

87. 6. Diagnosis A. History and physical examination:
Maternal risk factors, medications, birth and feeding history.
Physical examination should include a search for abnormal neurological signs and signs of sepsis.
B. Laboratory studies:
Complete septic workup, and screening for metabolic disorders.
C. Imaging and other studies:
Imaging for atelectasis, pneumonia, air leak, and NEC.
Cranial ultrasound to detect intracranial hemorrhage or congenital abnormalities.
Electroencephalogram (EEG) to rule out seizures, as apnea may be the sole presentation of seizures.

88. 7. Management. A- Pharmacologic management: Methylxanthine therapy.
Caffeine, theophylline, and aminophylline have been used as effective respiratory stimulants to decrease apnea of prematurity.
Methylxanthines increase minute ventilation, improve CO2 sensitivity, decrease hypoxic depression, enhance diaphragmatic activity, and decrease periodic breathing.
Initially, theophylline was the standard of treatment and required close monitoring of serum levels.

89. Common side effects include tachycardia, feeding intolerance, emesis, jitteriness, restlessness, and irritability.
Toxic effects may produce arrhythmias and seizures.
Caffeine has substantially fewer side effects, is better tolerated, and has a high therapeutic index when compared to theophylline.
Caffeine has a long half-life, which makes for a convenient once-a-day dosing regimen, and monitoring of caffeine levels at the recommended dosing is seldom necessary.

90. 2. Doxapram.
Doxapram is a potent nonspecific respiratory stimulant It stimulates peripheral chemoreceptors at low dose and central chemoreceptors at high dose.
Small doses are used for the treatment of AOP.
Doxapram increases tidal volume and minute ventilation. Studies have shown the effectiveness of doxapram in reducing apnea when refractory to methylxanthines.
As a result of poor absorption, it is used as a continuous intravenous infusion.
Side effects include an increase in blood pressure, abdominal distension, irritability, jitteriness, increased gastric residuals, and emesis.

91. Non- pharmacologic management
Prone, and head elevated positioning.
Prone position along with head elevated tilt position showed reduction in apnea and bradycardia.
b. Continuous positive airway pressure (CPAP).
CPAP at 4–6 cm H2O has proven to be a safe and effective therapy of apnea of prematurity. It is effective in obstructive apnea rather than central apnea.
c. Flow through nasal cannula.
Both high and low flow through nasal cannula can be a useful adjunct therapy in some infants with apnea who are already receiving methylxanthines.
d. Synchronized nasal ventilation.
Nasal intermittent positive pressure ventilation (N-IPPV). It seems to be more effective than CPAP in preventing extubation failure.

92. 8. Prognosis. Apnea of prematurity resolves with maturation.
The physiological basis for resolution of apnea is believed to be myelination of the brainstem.
It is important to distinguish the cause of the apnea from its effect. There is an association between recurrent apnea and later cerebral palsy,
Otherwise, in most infants apnea resolves without the occurrence of long-term deficiencies.

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