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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD.
Acute respiratory distress syndrome (ARDS) has some similarities to IRDS. Transient tachypnea of the newborn presents with respiratory distress syndrome in the preterm newborn.
Giving the mother glucocorticoids speeds the production of surfactant. For very premature deliveries, a glucocorticoid is given without testing the fetal lung maturity. The American College of Obstetricians and Gynecologists (ACOG), Royal College of Medicine, and other major organizations have recommended antenatal glucocorticoid treatment for women at risk for preterm delivery prior to 34 weeks of gestation. Multiple courses of glucocorticoid administration, compared with a single course, does not seem to increase or decrease the risk of death or neurodevelopmental disorders of the child.
In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid by amniocentesis, wherein a needle is inserted through the mother's abdomen and uterus. Several tests are available that correlate with the production of surfactant. These include the lecithin-sphingomyelin ratio ("L/S ratio"), the presence of phosphatidylglycerol (PG), and more recently, the surfactant/albumin (S/A) ratio. For the L/S ratio, if the result is less than 2:1, the fetal lungs may be surfactant deficient. The presence of PG usually indicates fetal lung maturity. For the S/A ratio, the result is given as mg of surfactant per gm of protein. An S/A ratio 55 indicates mature surfactant production(correlates with an L/S ratio of 2.2 or greater).
The mortality rate of meconium-stained infants is considerably higher than that of non-stained infants; meconium aspiration used to account for a significant proportion of neonatal deaths. Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to five to ten years. The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension. Fifty percent of newborns affected by meconium aspiration would die fifteen years ago; however, today the percent has dropped to about twenty.
In a study conducted between 1995 and 2002, MAS occurred in 1,061 of 2,490,862 live births, reflecting an incidence of 0.43 of 1,000. MAS requiring intubation occurs at higher rates in pregnancies beyond 40 weeks. 34% of all MAS cases born after 40 weeks required intubation compared to 16% prior to 40 weeks.
Type 1 respiratory failure is defined as a low level of oxygen in the blood (hypoxemia) without an increased level of carbon dioxide in the blood (hypercapnia), and indeed the PCO may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. The basic defect in type 1 respiratory failure is failure of oxygenation characterized by:
This type of respiratory failure is caused by conditions that affect oxygenation such as:
- Low ambient oxygen (e.g. at high altitude)
- Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism)
- Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe
- Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia or ARDS)
- Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt)
Hypoxemia (PaO2 6.0kPa).
The basic defect in type 2 respiratory failure is characterized by:
Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the buildup of carbon dioxide levels (PCO) that has been generated by the body but cannot be eliminated. The underlying causes include:
- Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation)
- Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
- A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
- Neuromuscular problems (Guillain–Barré syndrome, motor neuron disease)
- Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.
There is evidence to show that steroids given to babies less than 8 days old can prevent bronchopulmonary dysplasia. However, the risks of treatment may outweigh the benefits.
It is unclear if starting steroids more than 7 days after birth is harmful or beneficial. It is thus recommended that they only be used in those who cannot be taken off of a ventilator.
Sixty percent of people with acute interstitial pneumonitis will die in the first six months of illness. The median survival is 1½ months.
However, most people who have one episode do not have a second. People who survive often recover lung function completely.
In the United States, intrauterine hypoxia and birth asphyxia were listed together as the tenth leading cause of neonatal death.
Acute interstitial pneumonitis occurs most frequently among people older than forty years old. It affects men and women equally. There are no known risk factors; in particular, smoking is not associated with increased risk.
The prevalence of pulmonary interstitial emphysema widely varies with the population studied. In a 1987 study 3% of infants admitted to the neonatal intensive care unit (NICU) developed pulmonary interstitial emphysema.
When infants have a lower birth weight or younger gestational age, there is a greater risk of infantile apnea. With the advancement of neonatal intensive care units and the greater technology available, there are more successful premature births compared to the past. With the greater number of premature infants being born, there is also a greater number of children with infantile apnea. Approximately 85 percent of infants born with a weight less than experience infantile apnea within the first month after birth. This risk decreases to 25 percent for infants weighing less than . Studies have found that almost 2% of the pediatric population experience obstructive sleep apnea.
IH/BA is also a causitive factor in cardiac and circulatory birth defects the sixth most expensive condition, as well as premature birth and low birth weight the second most expensive and it is one of the contributing factors to infant respiratory distress syndrome (RDS) also known as hyaline membrane disease, the most expensive medical condition to treat and the number one cause of infant mortality.
In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in "Pa"CO. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
- Acute respiratory acidosis: HCO increases 1 mEq/L for each 10 mm Hg rise in "Pa"CO.
- Chronic respiratory acidosis: HCO rises 3.5 mEq/L for each 10 mm Hg rise in "Pa"CO.
The expected change in pH with respiratory acidosis can be estimated with the following equations:
- Acute respiratory acidosis: Change in pH = 0.008 X (40 − "Pa"CO)
- Chronic respiratory acidosis: Change in pH = 0.003 X (40 − "Pa"CO)
Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.
Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.
Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial lung disease and thoracic deformities.
Lung diseases that primarily cause abnormality in alveolar gas exchange usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs.
Studies reflecting international frequency demonstrated that 2-3% of all infants in NICUs develop pulmonary interstitial emphysema. When limiting the population studied to premature infants, this frequency increases to 20-30%, with the highest frequencies occurring in infants weighing fewer than 1000 g.
Pulmonary diseases may also impact newborns, such as pulmonary hyperplasia, pulmonary interstitial emphysema (usually preterm births), and infant respiratory distress syndrome,
Respiratory disease is a common and significant cause of illness and death around the world. In the US, approximately 1 billion "common colds" occur each year. A study found that in 2010, there were approximately 6.8 million emergency department visits for respiratory disorders in the U.S. for patients under the age of 18. In 2012, respiratory conditions were the most frequent reasons for hospital stays among children.
In the UK, approximately 1 in 7 individuals are affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease, which includes asthma, chronic bronchitis and emphysema.
Respiratory diseases (including lung cancer) are responsible for over 10% of hospitalizations and over 16% of deaths in Canada.
In 2011, respiratory disease with ventilator support accounted for 93.3% of ICU utilization in the United States.
Fetal mortality refers to stillbirths or fetal death. It encompasses any death of a fetus after 20 weeks of gestation or 500 gm. In some definitions of the PNM early fetal mortality (week 20-27 gestation) is not included, and the PNM may only include late fetal death and neonatal death. Fetal death can also be divided into death prior to labor, antenatal (antepartum) death, and death during labor, intranatal (intrapartum) death.
Preterm birth is the most common cause of perinatal mortality, causing almost 30 percent of neonatal deaths. Infant respiratory distress syndrome, in turn, is the leading cause of death in preterm infants, affecting about 1% of newborn infants. Birth defects cause about 21 percent of neonatal death.
A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.
In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death.
Mixed apnea is a combination of both central and obstructive factors. The majority of premature infants with sleep apnea have mixed apnea.
Injury to the lung may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include:
- Inhalation of hot or toxic gases
- Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)
- Aspiration, e.g., gastric fluid
- Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.
- Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
- Swimming induced pulmonary edema also known as immersion pulmonary edema
- Transfusion Associated Circulatory Overload (TACO) occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time.
- Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the donor, such as anti-HLA or anti-neutrophil antibodies.
- Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS.
Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above.
- Arteriovenous malformation
- Hantavirus pulmonary syndrome
- High altitude pulmonary edema (HAPE)
- Envenomation, such as with the venom of Atrax robustus
Perinatal asphyxia, neonatal asphyxia or birth asphyxia is the medical condition resulting from deprivation of oxygen to a newborn infant that lasts long enough during the birth process to cause physical harm, usually to the brain. Hypoxic damage can occur to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to quickly or completely heal. In more pronounced cases, an infant will survive, but with damage to the brain manifested as either mental, such as developmental delay or intellectual disability, or physical, such as spasticity.
It results most commonly from a drop in maternal blood pressure or some other substantial interference with blood flow to the infant's brain during delivery. This can occur due to inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. Perinatal asphyxia happens in 2 to 10 per 1000 newborns that are born at term, and more for those that are born prematurely. WHO estimates that 4 million neonatal deaths occur yearly due to birth asphyxia, representing 38% of deaths of children under 5 years of age.
Perinatal asphyxia can be the cause of hypoxic ischemic encephalopathy or intraventricular hemorrhage, especially in preterm births. An infant suffering severe perinatal asphyxia usually has poor color (cyanosis), perfusion, responsiveness, muscle tone, and respiratory effort, as reflected in a low 5 minute Apgar score. Extreme degrees of asphyxia can cause cardiac arrest and death. If resuscitation is successful, the infant is usually transferred to a neonatal intensive care unit.
There has long been a scientific debate over whether newborn infants with asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.
There is considerable controversy over the diagnosis of birth asphyxia due to medicolegal reasons. Because of its lack of precision, the term is eschewed in modern obstetrics.