In recent years increasingly
relevant bronchopulmonary dysplasia (BPD).
acquired chronic obstructive pulmonary disease that develops as a result of
respiratory distress syndrome of neonates and / or artificial ventilation (AVL)
with high concentrations of oxygen, accompanied by hypoxemia, altered
reactivity of the bronchi with hypersensitivity of airways, and typical
In the etiology
of BPD there are many factors: the impact of oxygen in high concentrations,
mechanical ventilation, pulmonary edema, left to right shunt at patent ductus
arteriosus, recurrent bacterial pneumonia, hereditary predisposition,
hypovitaminosis A and E.
Anatomy and Physiology
According to the results of
postmortem studies, there are 4 stages of BPD, which are similar to roengenologic
findings. In the first three days of life (I stage), there is a typical
respiratory distress syndrome. In the following days the first week of life (II
stage) there are destruction of cells of the alveolar epithelium and capillary
endothelium, interstitial edema and perivascular space, necrosis of the
bronchioles, squamous metaplasia, hypertrophy of smooth muscle cells of the
disappearance of ciliated epithelium. In the II-III week (III stage) there is increasing
of the number of macrophages and plasma cells and fibroblasts. Process damage
the bronchial tubes of different orders, which in severe cases leads to obliterative
bronchiolitis. In the following week
atelectasis zones with interstitial and peribronchial fibrosis in conjunction
with areas of emphysema (IV stage) are revealed. In the walls of the alveoli there
is increasing of the number of reticular, collagen, elastic fibers, which
structure is disrupted.
Naturally pulmonary emphysema
develops caused by three mechanisms: 1) scars that appear due to hyperextension
of nonfibroid lung; 2) violation of the multiplication of alveoli in some areas
(atrophic form of emphysema); 3) destruction as a result of the inflammation
and destruction of the walls of the alveoli and capillaries. Structural changes
of the pulmonary arteries include intimal proliferation, smooth muscle
hypertrophy, the proliferation of smooth muscle on the distal parts of vessels,
thickening and fibrosis of the adventitia, the decreasing of diameter of the
In diagnosing BPD
anamnestic data are important:
·birth weight less than 1500g
·RDS in the first hours of life
·ALV with rigid parameters for more
than 6 days
·oxygen dependance at least 1 month.
Specific clinical manifestations of
BPD are absent. The clinical picture of BPD symptoms is presented with chronic
respiratory failure (tachypnea to 80-100 per minute, cyanosis, emphysema, rib
retraction, persistent physical examination changes in the form of an elongated
exhalation, dry wheezing, moist small bubbling rales, stridor is possible) in
preterm infants who are dependent on high concentrations of oxygen in inhaled
air and mechanical ventilation for a longer or shorter time.
Resistant respiratory failure
develops after the initial improvement under AVl. This dependence on oxygen and
mechanical ventilation may be manifested in different ways.
The diagnosis of BPD brings together
a wide range of clinical manifestations and changes on the radiograph. In mild
cases may be observed only the impossibility of reducing the oxygen concentration
and the parameters of artificial ventilation for 1-2 weeks, lengthening the
period of recovery from respiratory failure. In severe cases in the background
of AVL hypoxemia, hypercapnia remain, "remove" a child from a
ventilator is impossible within a few months, reintubations are characteriatic.
Typically, the suspicion of BPD occur when the child needed mechanical ventilation,
especially with positive end-expiratory pressure, for more than 1 week. Cough,
persistent symptoms of bronchial obstruction syndrome in patients are preserved
on already spontaneous respiration.
Further, after the neonatal period, course
of BPD is wavy, depending on the degree of morphological and functional
disorders. The majority of patients showed a slow but clear improvement and
normalization of the state in 6-12 months, but in some patients violations
persist for a long time. According to observations GM Dementieva et al. (1997)
at 16-20% of children discharged from office for prematurity, pathological changes
in the lungs retained and in older age - for 1-4 years of life, and 4% of
patients BPD in the future lead to disability. Recovery in children with BPD
may be due to the fact that along with the fibro-proliferative processes in the
lungs of preterm there is occurring regenerative process and continuing growth
and development of the lungs.
Examination reveals the cough and
persistent physical examination changes, the increasing of obstructive
disorders at virus infection, the symptoms of latent respiratory insufficiency
detected by the load - sucking, moving, crying, while often develop pulmonary
heart at an early age, neurological disorders, retarded physical development.
The final diagnosis is established after the radiographic examination with
signs of fibrosis in the form of deformation and strengthening of local lung
pattern or a light disguise lung fields in middle medium sections, alternating
with areas of swelling of lung tissue, primarily in low lateral areas in
children older than 1 month.
of child 5 mths with BPD
Activities for the prevention of BPD include:
Pharmacological acceleration of lung maturation: prenatal prevention of RDS
accelerates the maturation of surfactant synthesis and is one of effective
methods of reducing the frequency and severity of BPD. Birth of a baby without
the RDS gives possible to avoid
mechanical ventilation, and consequently, the mechanical (positive pressure)
and chemical (oxygen) injury of the lungs. One of the most common methods of
prenatal prevention of RDS is the GCS therapy, which stimulates the synthesis
of surfactant in the lungs of the fetus.
etiopathogenic therapy of RDS: in preterm infants it involves the use of
exogenous surfactant preparations that can achieve the reduction of severity
and reducing the duration of the disease and, consequently, the duration of
mechanical ventilation and oxygen therapy in general.
of the optimal level of respiratory support of child: currently there is no doubt that the
early onset of respiratory care can reduce its duration and limit the softer
options like the pressure and the oxygen content. Early spontaneous respiration
under constant positive pressure of (SRCPP) makes it possible to limit the scope
of respiratory care, stop the progression of RDS and avoid the need for
At mechanical ventilation it should
be strive to limit the minimal sufficient level of peak pressure and minimal
sufficient concentration of oxygen. A special problem is a return the child from
mechanical ventilation to spontaneous respiration. This is a long process,
involving a slow decrease in ventilatory parameters, transfer the child to SRCPP
through endotracheal tube, and then - through a nasal cannula.
maintenance of water balance and energy supplementation: control of water
balance is reduced to restrict fluids to 90% of fluid consumption. Excessive
hydration leads to the pulmonary edema and disorders of gas exchange.
Already in the early stages of BPD
children need increased energy supply. Parenteral nutrition in the first days
of life is intended to prevent catabolic processes. The full parenteral
providing of proteins, carbohydrates, fats, vitamins and micro elements is
important to limit further damage to the lungs and create conditions for their
In children with already
established BPD in terms of water balance, their treatment has a number of perculiarities.
Children with BPD have little resistant to the normal amount of fluid and tend
to accumulate it in their lungs. They haveproblems with nutrition, manifested in an imbalance between the demand of
food and limitation of fluid. Often grows retardation occurs, so calloriesshould be increased, due to immaturity, growth
need, increased work of breathing, high levels of metabolism (the additional
cost of the energy supply of the inflammatory reaction). In order to achieve
normal growth and development there must be at least 120-150 kcal / kg per day.
5. Supply of
antioxidant protection. There is the immaturity of enzyme mechanisms in preterm
infants. Animal studies and human biological material confirm the effectiveness
of superoxide dismutase and catalase, the result of which is manifested
decreasing of cell damage, increasing survival, and possibly the prevention or
reduction in the severity of barotrauma. Today GCS are used n the postnatal
period, not only for prevention of BPD, but for treatment of already formed
1. System GCS
stabilize cellular and lysosomal membranes, increases surfactant synthesis,
increases the concentration of vitamin A in serum, inhibit prostaglandins and
leukotrienes, reduce swelling of lung tissue and improve microcirculation in
it. Currently, there is intensive studing of the role of inhaled GCS
(beclomethasone, budesonide, flyuticazon) as an alternative to systemic GCS, or
as a component of systemic steroid therapy. The available data are contradictory:
some researchers prefer inhalation dexamethasone, others do not confirm the
benefits of its application.
Steroid therapy involves
two options: early administration of steroids prevents the formation of BPD
(late first - early second week of life when on the background of persistent
pulmonary edema appears interstitial emphysema) andtreats already established BPD (from the
second month of life). Routine use of dexamethasone in the treatment of BPD is
not currently recommended because of the many negative side effects. Its
appointment is justified only when there is extreme severity of pulmonary
2. Inhaled β2-adrenomimetics also found
their application in the treatment of BPD. Salbutamol is a specific agonist of
β2-receptors and currently enjoys high popularity in the
treatment of BPD. Thanks bronchodilatory effect it reduces bronchial resistance
and increases the permeability of the bronchi. However, since the first weeks
of life expressed relaxation of smooth muscles of the bronchi is absent, early
salbutamol inhalation therapy is not considered justified.
bronchodilators, which are the most commonly used in the treatment of children
with BPD, include methylxanthines - aminophylline, theophylline, caffeine (more
4. Pulmonary vasodilators: nifedipine (calcium channel
blockers). A single oral dose of nifedipine (0.5 mg / kg) reduces vascular
resistance in the lungs and increases cardiac output in older children with
severe vascular hypertension due to BPD.
5. Antibiotic: A number of studies in recent years
distinguished Ureoplasma urealyticum as a factor contributing to the
development of BPD. The results of clinical trials demonstrate reduction in the
severity of the disease during therapy with macrolides.