Transcript for Neonatal ICU
Preterm infants sometimes develop life-threatening complications that require immediate Neonatal ICU admission and management.
Some common issues that occur in a preterm infant include intraventricular hemorrhage, retinopathy of prematurity, apnea of prematurity, bronchopulmonary dysplasia, persistent pulmonary hypertension of the newborn, respiratory distress syndrome, feeding difficulties, gastroesophageal reflux disease, necrotizing enterocolitis, neonatal jaundice, and fetal growth restriction.
Now, prematurity is defined as a birth that occurs before 37 completed weeks of gestation.
The different degrees of prematurity can be defined by gestational age and birth weight.
The classification based upon gestational age is as follows: late preterm birth is when the gestational age is between 34 and less than 37 weeks; moderate preterm birth is between 32 and less than 34 weeks; very preterm birth is under 32 weeks; and extremely preterm birth - when the gestational age is below 28 weeks.
The birth weight classification is as follows: low birth weight is when the baby weighs less than 2500 grams, very low birth weight is under 1500 grams; and extremely low birth weight is when the baby weighs less than 1000 grams.
First, in intraventricular hemorrhage, bleeding in the germinal matrix occurs within the first day after birth.
The germinal matrix is located between the caudate nucleus and the thalamus, at the level of the foramen of Monro.
The etiology is multifactorial but it’s primarily attributed to vascular fragility and to disturbances in cerebral blood flow.
On examination, there are three possible presentations in the preterm infant. First, the silent presentation is detected by routine ultrasound screening.
Second, the saltatory or stuttering course evolves over hours to several days and it’s characterized by nonspecific findings, like altered consciousness, hypotonia, and abnormal eye movements and position. The respiratory function is can also be affected, resulting in respiratory distress.
And third, catastrophic deterioration is rare and evolves over minutes to hours. Signs include stupor or coma; irregular respirations, hypoventilation, or apnea; generalized seizures, especially tonic seizures; and flaccid weakness. A bulging anterior fontanelle, hypotension, and bradycardia might also be part of the clinical picture.
Next, the diagnosis is confirmed by cranial ultrasound. It usually detects blood in the lateral ventricles with subsequent dilatation; secondary hydrocephalus- a condition where cerebrospinal fluid accumulates in the brain; and in severe cases, it might associate areas of infarction.
Because intraventricular hemorrhages are mostly clinically silent, routine ultrasound screening should be performed in all preterm infants with a gestational age under 30 weeks on the first day of admission.
If the ultrasound is inconclusive but there’s a strong clinical suspicion, an MRI is needed to identify small hemorrhages and any associated lesions in the white matter and cerebellum.
If both are unavailable, a lumbar puncture and cerebrospinal fluid analysis can be performed to assist diagnosis.
However, lumbar puncture must be performed cautiously because there’s a risk of herniation in infants with large unilateral or posterior fossa hemorrhages.
In intraventricular hemorrhage, the cerebrospinal fluid typically contains numerous red blood cells and a high protein concentration. It also becomes xanthochromic several hours after the hemorrhage, and its glucose concentration may be reduced.
Regarding treatment, there is no specific therapy for this condition.
Supportive management is directed towards preservation of cerebral perfusion, minimization of any further brain injury, and early detection of complications.
For example, it can include delaying cord clamping for 60 seconds to increase the newborn’s blood flow, ensuring respiratory support when and if needed, and correction of any metabolic disturbance that might arise.
Additionally, data shows antenatal corticosteroids given before preterm birth can reduce the risk of intraventricular hemorrhage.
Second is retinopathy of prematurity. It is a vascular disorder that occurs in the retina of preterm infants, leading to severe visual impairment.
Now, the inner retinal blood vessels start growing at 15 to 18 weeks of gestation but the retina is not fully vascularized until term.
Sometimes, in a preterm infant, the retinal vessels continue their growth in an abnormal pattern, which results in a ridge of tissue between the vascularized central retina and the nonvascularized peripheral retina.
The exact cause is unknown but hypotension, hypoxia, or hyperoxia have all been incriminated.
On examination, individuals appear normal but vision loss might occur as the child grows. This means the diagnosis is based solely on ophthalmoscopic examination, where the retina is examined by looking through the pupil with an indirect ophthalmoscope using a 20 or 28 diopter condensing lens.
Ophthalmoscopy can detect any abnormal growth pattern of the blood vessels in the retina and categorize the condition based on the lesion’s position relative to the optic nerve.
Screening by ophthalmoscopy is done in all infants weighing under 1500 grams or under 30 weeks gestation at birth.
Ophthalmologic examinations continue every 1 to 3 weeks until the retina starts to look normal.
Therapy-wise, severe cases can be managed by laser photocoagulation, which can ablate the peripheral avascular retina and reduce the risk of complications like retinal detachment.
Now, if retinal detachments do occur, scleral buckling surgery or vitrectomy with lensectomy may be considered.
As 2nd-line therapy, bevacizumab, an anti-vascular endothelial growth factor monoclonal antibody, can stop the progression of retinopathy of prematurity but has more side effects than laser photocoagulation.
Third, apnea of prematurity is a developmental disorder of the preterm infant characterized by breathing pauses.
The causes are poorly understood but abnormal responses to hypoxia and hypercapnia, obstructed airflow, or reflex laryngospasm are thought to contribute to its development.
On examination, preterm infants usually develop apneic spells one or two days after they’re born, which can help establish the diagnosis.
Apneic spells are respiratory pauses of at least 20 seconds or pauses under 20 seconds that are associated with bradycardia - usually 80 beats per minute, cyanosis, and/or pallor.
Next, pulse oximetry monitoring can be used to measure the oxygen saturation and heart rate of the newborn.
In apnea of prematurity, the oxygen saturation is typically under 85% and the heart rate under 80 beats per minute.
Treatment can begin with stimulation by drying the baby and rubbing the back or the soles of the feet.
Additionally, they can be placed on a radiant warmer or incubator to preserve heat loss; have any secretion suctioned from the nose and mouth; and have their head and neck in a neutral position.
If breathing does not resume, bag-valve-mask or mouth-to-mouth-and-nose ventilation must be provided.
Frequent or severe episodes, characterized by hypoxemia, cyanosis, bradycardia, or a combination, can be managed with oral or intravenous caffeine.
Caffeine is usually administered as citrate, and it acts as a respiratory stimulant drug with a loading dose of 20 milligrams per kilogram followed by a maintenance dose of 5 to 50 milligrams per kilogram every 24 hours.
Treatment continues until the infant is 34 to 35 weeks of gestation and free from apnea for at least 5 to 7 days.
Monitoring continues until the infant is free of apnea requiring intervention for 5 to 10 days.
If apnea continues despite respiratory stimulants, the infant may be given CPAP starting at 4 to 6 centimeters water pressure.
Next, bronchopulmonary dysplasia, also known as neonatal chronic lung disease, is caused by abnormal pulmonary development, usually as a result of prolonged mechanical ventilation.
Some of the changes that occur are a decrease in alveoli number, interstitial thickening, abnormal development of the pulmonary vasculature, pulmonary edema, and atelectasis.
Now, on examination, the condition presents as respiratory distress.
Additionally, depending upon the extent of pulmonary edema and atelectasis, individuals might have mild to severe retractions and scattered rales may also be audible.
Intermittent expiratory wheezing is possible in those with airway narrowing from scar formation, constriction, mucus retention, collapse, or edema.
Most of the time, a diagnosis can be established based on clinical findings.
More specifically, it is based on the need for oxygen supplementation at 36 weeks postmenstrual age, which is gestational age plus chronologic age.
For example, an infant with a gestational age of 26 weeks and a chronologic age of 6 weeks would have a postmenstrual age of 32 weeks.
Next, there are a few tests that can be performed to help establish the diagnosis.
First, an oxygen reduction test can be performed to define the actual need for oxygen supplementation.
Diagnosis is confirmed if the oxygen saturation falls below 90 percent within 60 minutes of being placed in room air.
Next, a chest radiograph is recommended to assess the extent of the disease.
Usual findings include diffuse haziness due to the accumulation of exudative fluid; and a multicystic or sponge-like appearance, with alternating areas of emphysema, pulmonary scarring or edema.
Later in evolution, there may be areas of atelectasis that alternate with areas of gas trapping secondary to airway obstruction from secretions.
Treatment is supportive and it combines nutritional supplementation, fluid restriction, diuretics, and oxygen supplementation.
Respiratory infections must be diagnosed early and treated aggressively to prevent further pulmonary damage.
Feedings should achieve an intake of 150 calories per kilogram a day, including protein 3.5 to 4 grams per kilogram; this is needed because of the increased work of breathing and to aid lung healing and growth.
Because pulmonary congestion and edema may develop, daily fluid intake is often restricted to about 120 to 140 milligrams per kilograms a day.
Chlorothiazide 10 to 20 milligrams per kilogram per day with or without spironolactone is often tried first.
Ok so persistent pulmonary hypertension of the newborn occurs when the pulmonary vascular resistance doesn’t decrease as it should after birth.
The condition may be idiopathic or secondary to certain neonatal pulmonary diseases, including congenital diaphragmatic hernia, respiratory distress syndrome, meconium aspiration syndrome, and transient tachypnea of the newborn.
On presentation, symptoms include tachypnea, retractions, and severe cyanosis or desaturation unresponsive to oxygen.
Next, diagnosis is confirmed by echocardiogram, which shows elevated pressures in the pulmonary artery.
Pulse oximetry is used in conjunction with echocardiography and it typically shows a difference of more than 10 percent between the pre- and postductal oxygen saturation, which is the saturation measured at the right thumb and either great toe.
This occurs due to right-to-left shunting through the patent ductus arteriosus.
However, the absence of a pre- and postductal gradient in oxygenation does not exclude the diagnosis of persistent pulmonary hypertension of the newborn, because right-to-left shunting can occur predominantly through the foramen ovale rather than the patent ductus arteriosus.
Additionally, other tests might be needed if echocardiography is inconclusive.
Blood cultures are typically normal, which helps eliminate pneumonia as a possible cause of persistent pulmonary hypertension in the newborn.
Chest x-ray is usually normal too or it might reveal an associated or causing pulmonary condition.
Treatment begins with oxygen supplementation, which acts as a pulmonary vasodilator.
Oxygen is usually delivered via bag-and-mask or mechanical ventilation.
In severe cases or when symptoms don’t improve, further interventions include the use of vasodilatory agents like inhaled nitric oxide.
Nitric oxide relaxes the endothelial smooth muscle and dilates the pulmonary arterioles, which increases pulmonary blood flow and rapidly improves oxygenation.
The initial dose is 20 parts per million, titrated downward by effect.
If nitric oxide therapy fails the last option is extracorporeal membrane oxygenation, which is a machine that temporarily replaces the function of the heart and lung.
Sixth, respiratory distress syndrome is caused by a deficiency of surfactant, the phospholipid mixture that reduces alveolar surface tension to keep the alveoli inflated and maintains alveolar stability. This prevents the infant from generating the increased inspiratory pressure needed to inflate alveolar units, resulting in the development of progressive and diffuse atelectasis.
On examination, the clinical picture is of a preterm infant with the onset of progressive respiratory failure shortly after birth.
Next, chest radiography usually shows low lung volume and the classic diffuse reticulogranular ground glass appearance with air bronchograms resulting from alveolar atelectasis contrasting with aerated airways.
Arterial blood gasses usually show hypoxemia and hypercapnia.
Regarding treatment, antenatal corticosteroid therapy should be administered to all pregnant individuals at 23 to 34 weeks gestation who are at increased risk of preterm delivery to prevent or decrease the severity of neonatal respiratory distress syndrome.
In newborns without respiratory failure, nasal continuous positive airway pressure is the preferred initial intervention. If this fails and apnea develops, the infant requires endotracheal intubation and intratracheal surfactant therapy with poractant alfa, calfactant, or beractan.
Another common issue in preterm infants is feeding difficulties due to sucking and swallowing disorders.
Normally, term newborns can extract milk from either the breast or bottle, which is called nutritive sucking; form a bolus of fluid and transport it through the upper digestive tract, which is swallowing; and prevent the food from getting in the airways or aerodigestive protection.
In the preterm infant, there are three main causes that can impair these processes or skills.
First is prematurity, where the feeding skills have not yet appeared because these mechanisms fully develop around 34 weeks of gestation.
Second, anatomical defects like cleft lip, diaphragmatic hernia, pyloric stenosis, and gastroschisis which is the congenital fissure of the abdominal wall, might make feeding impossible by obstructing the normal bolus pathway.
And third, neurological, neuromuscular, and neurodevelopmental disorders like hypoxic-ischaemic encephalopathy, cerebral palsy, spinal muscular atrophy, and myasthenia gravis might create a disruption in the coordination between the three processes or a congenital defect that results in ineffective feeding.
Now, on examination, preterm infants might not be able to suck milk out of the nipple or feeding bottle, swallow, and they might present dysphagia, drooling, and regurgitation. In severe cases, especially those associated with food aspiration, they could develop apnea, noisy breathing, bradycardia, failure to thrive, and cyanosis.
Next, in the ICU or nursery, a feeding assessment is performed to assess the individual’s pre-feeding skills; oral readiness or whether they can begin safe oral feeding; and their ability to breast and bottle-feed.
Evaluation of pre-feeding skills is an assessment meant to see if the infant can remain engaged in feeding, properly use the facial muscle to eat, coordinate swallowing with breathing, and regulate the depth and frequency of breathing to maintain physiologic stability.
Usually, premature infants under 32 weeks gestation are not mature enough to have developed these skills and cannot begin oral feeding.
Oral readiness criteria include medical stability, gestational age over 33 to 34 weeks, and the presence of a nonnutritive sucking and suction pattern - meaning the infant can properly use the pacifier.
Diagnosis of feeding difficulties due to prematurity can be established clinically in those under 32 weeks of gestation age with typical symptoms, and no sign of severity or of another pathology.
Next, further diagnostic evaluation is needed if another cause of feeding difficulty is suspected or if the clinical picture is severe enough to justify it.