In diagnosing bpd anamnestic data are important:

·        prematurity

·        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.

                                  Clinic:

            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.

Roentgenography of child 5 mths with BPD  

           Activities for the prevention of BPD include:

1. 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.

2. Rational 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.

3. Selection 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 mechanical ventilation.

               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.

4. Proper 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 repair.

              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 have  problems with nutrition, manifested in an imbalance between the demand of food and limitation of fluid. Often grows retardation occurs, so callories  should 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 disease.

                            Therapeutic activities:

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.  

Flixotide

                    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) and  treats 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 symptoms.

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.

3. Systemic bronchodilators, which are the most commonly used in the treatment of children with BPD, include methylxanthines - aminophylline, theophylline, caffeine (more rarely).

  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.

                         BRONCHIAL ASTHMA

Bronchial asthma is a disease manifested reversible (fully or partially), bronchial obstruction, which is based on pathogenetic allergic inflammation of airways and, in most cases, bronchial hyperreactivity.

It is characterized by recurring attacks of breathlessness, resulting from smooth muscle spasm, edema of mucous membrane of the bronchi and their blockage by viscid secret that leads to the BOS.

                                       Etiology and pathogenesis.

                   Asthma may be allergic origin, ie, occurs in individuals with increased sensitivity to certain chemicals or physical factors - allergens. Increased sensitivity may be a manifestation of hereditary-constitutional features of the organism, or develops as a result of prolonged contact with the allergen, while the impact on the body of a number of adverse factors (cooling, fatigue, chronic inflammatory diseases, etc.).

                  Asthma may also be infectious origin. At the outbreak of infectious bronchial asthma important role have bacteria, viruses and other microbes, which in interaction with the organism cause its allergic restruction. Most often it develops on a background of chronic respiratory diseases or paranasal sinusitis, at which in the body there is infection focus of a long time, as well as products of the microbes and substances produced during inflammation, have the properties of allergens.

              Noninfectious asthma is caused by allergens of animal and vegetable origin. Allergens of animal origin include wool, horse hair, fish scales, etc. Sensitivity is sometimes also observed in some insect - bugs, cockroaches, butterflies, etc. Among the allergens of plant pollens play a special role. Bronchial asthma caused by plant allergens occur in a certain season of the year (April - July) - the period of flowering plants. In addition, the cause of asthma may be house dust and dry food for aquarium fish, etc., certain foods (eggs, crabs, chocolate, mushrooms, strawberries, oranges, etc.), some medicines.

             In the event of attack of asthma there are importance of  individual characteristics of nervous and endocrine systems. There are known occasions that in  the patient with sensitiveness to the smell of roses, attack started at the sight of artificial roses. Negative emotions may provoke attacks also. In some patients attacks of asthma do not appear in periods of intense work, or during deep sleep.

             The development and course of bronchial asthma depend on climatic factors. Exacerbations of the disease are often observed in spring and fall moon, patients often feel worse in windy weather, with sudden changes in temperature and atmospheric pressure at high humidity. In addition, high humidity contribute to the exacerbation of chronic bronchial and lung infections, which aggravates the course of bronchial asthma.

             The modern theory of the pathogenesis of asthma is the concept of allergic inflammation, which has become an integrating, connecting the mediator (histamine), lipid membranes - receptor (β2 - adrenergic receptors), neurovegetative (vagotonia), reagine (Ig E) and other concepts. Development of suffocation is conditioned directly by three major pathophysiological mechanisms: bronchospasm, edema of bronchial mucosa and hypersecretion of bronchial glands.                      

The inflammatory response in asthma is illustrated in this airway section from a patient with mild asthma who died in an accident. There is a submucosal infiltration of eosinophils and a marked deposition of collagen below the basement membrane. (From Hilman BC (ed): Pediatric Respiratory Disease. Philadelphia, WB Saunders, 1993, p.625.)                

                                                 Classification of bronchial asthma

               The severity of asthma is classified on the basis of complex clinical and functional signs of bronchial obstruction. The physician evaluates the frequency, severity and duration of attacks of expiratory dyspnea, patient's condition during the period between attacks, severity, variabillity, and repayment of functional bronchial obstruction, response to treatment. Evaluation of functional indicators for determining the severity of the disease is carried out in the absence of episodes expiratory dyspnea. According to this classification, the patient's condition is determined by the degrees of seriousness of bronchial asthma. So there are  intermittent (episodic) course; persistent (constant) course: mild, moderate and severe.

                The National Asthma Education and Prevention Program Expert Panel Report II (EPR-2), "Guidelines for the Diagnosis and Management of Asthma," highlight the importance of correctly diagnosing asthma. To establish the diagnosis of asthma, the clinician must establish the following: (a) episodic symptoms of airflow obstruction are present, (b) airflow obstruction or symptoms are at least partially reversible, and (c) alternative diagnoses are excluded.

                  The severity of asthma is classified as mild intermittent, mild persistent, moderate persistent, or severe persistent, according to the frequency and severity of symptoms, including nocturnal symptoms, characteristics of acute episodes, and pulmonary function.

                 These categories do not always work well in children. First, lung function is difficult to assess in younger children. Second, asthma that is triggered solely by viral infections does not fit into any category. While the symptoms may be intermittent, they may be severe enough to warrant hospitalization. Therefore, a category of severe intermittent asthma has been suggested.

                           Features of the categories include the following:

                 Patients with mild intermittent disease have symptoms fewer than 2 times a week, and pulmonary function is normal between exacerbations. Exacerbations are brief, lasting from a few hours to a few days. Nighttime symptoms occur less than twice a month. The variation in peak expiratory flow (PEF) is less than 20%.

             Patients with mild persistent asthma have symptoms more than 2 times a week but less than once a day. Exacerbations may affect activity. Nighttime symptoms occur more than twice a month. Pulmonary function test results (in age-appropriate patients) demonstrate that the forced expiratory volume in 1 second (FEV1) or PEF is less than 80% of the predicted value, and the variation in PEF is 20-30%.

              Patients with moderate persistent asthma have daily symptoms and use inhaled short-acting beta2-agonists every day. Acute exacerbations in patients with moderate persistent asthma may occur more than 2 times a week and last for days. The exacerbations affect activity. Nocturnal symptoms occur more than once a week. FEV1 and PEF values are 60-80% of the predicted values, and PEF varies by more than 30%.

             Patients with severe persistent asthma have continuous or frequent symptoms, limited physical activity, and frequent nocturnal symptoms. FEV1 and PEF values are less than 60% of the predicted values, and PEF varies by more than 30%.

             Disease with any of their features is assigned to the most severe grade. The presence of one severe feature is sufficient to diagnose severe persistent asthma. The characteristics in this classification system are general and may overlap because asthma is highly variable. The classification may change over time. Patients with asthma of any level of severity may have mild, moderate, or severe exacerbations. Some patients with intermittent asthma have severe and life-threatening exacerbations separated by episodes with almost normal lung function and minimal symptoms; however, they are likely to have other evidence of increased BHR (exercise or challenge testing) due to ongoing inflammation.

            Physical examination during an acute episode may reveal different findings in mild, moderately severe, and severe episodes and in status asthmaticus with imminent respiratory arrest.

Mild episode: The respiratory rate is increased. Accessory muscles of respiration are not used. The heart rate is less than 100 beats per minute. Pulsus paradoxus is not present. Auscultation of chest reveals moderate wheezing, which is often end expiratory. Oxyhemoglobin saturation with room air is greater than 95%.

Moderately severe episode: The respiratory rate is increased. Typically, accessory muscles of respiration are used, and suprasternal retractions are present. The heart rate is 100-120 beats per minute. Loud expiratory wheezing can be heard. Pulsus paradoxus may be present (10-20 mm Hg). Oxyhemoglobin saturation with room air is 91-95%.

Severe episode: The respiratory rate is often greater than 30 breaths per minute. Accessory muscles of respiration are usually used, and suprasternal retractions are commonly present. The heart rate is more than 120 beats per minute. Loud biphasic (expiratory and inspiratory) wheezing can be heard. Pulsus paradoxus is often present (20-40 mm Hg). Oxyhemoglobin saturation with room air is less than 91%.

Status asthmaticus with imminent respiratory arrest: Paradoxical thoracoabdominal movement occurs. Wheezing may be absent (associated with most severe airway obstruction). Severe hypoxemia may manifest as bradycardia. Pulsus paradoxus noted earlier may be absent; this finding suggests respiratory muscle fatigue.

                                                           Clinic

                  Asthma may be manifested in the form of whistles, wheezing when breathing, shortness of breath (dyspnea) with exertion or at rest, in the form of coughing, which may be paroxysmal.

                  The classic manifestation of bronchial asthma is the attack of asphyxia. Typically, it begins suddenly, usually at night. The patient feels a pain and lack of air. Breathing is difficult, exhaling long and is accompanied by a loud whistling wheezing (so-called, expiratory dyspnea). Cough may join soon. In order to facilitate breathing patient takes the forced position - rising or setting, leaning on the edge of the bed, chair, straining his pectoral muscle.                

                   After some time, breathing becomes calmer, sputum is separating; attack stops. Attacks last from several minutes to several hours or even days. Such prolonged or frequent (occurring at short intervals during the day) the attacks are called an asthmatic state. Occasional attacks do not leave behind any changes in the lungs, but with the development of the disease and the increasing frequency of attacks may occur emphysema, impairment of the heart. It should be in mind that asphyxia may be caused not only by asthma but other diseases. In most cases, the doctor during the examination of  the patient may determine the nature and origin of suffocation, with the need to use instrumental and laboratory methods.

                 Objectively: skinis pale, cyanosis of the lips, nasolabial triangle, acrocyanosis. Thorax is blown, shoulders are raised, lung percussion sound is bandbox, auscultation reveals relaxed breathing, prolonged exhaling, a large number of dry whistling wheezing and changing moist rales. Borders of the heart are not defined, the tones are weakened, tachycardia.

                        Diagnostic criteria

Anamnesis. Symptoms: wheezing, shortness of breath, cough, fever, the formation of phlegm, and other allergic disorders. There is possible presence of contributing factors (allergens, infection, etc.), occurrence of asthma attacks at night. Attacks are curable. The outcome of previous attacks (the need for hospitalization, treatment with steroids).

Physical examination. Total: tachypnea, tachycardia, part of the auxiliary respiratory muscles, cyanosis, paradoxical pulse (the inclusion of support muscles and paradoxical pulse are correlated with the severity of obstruction). Lungs: adequate aeration, with auscultation the symmetry of breath, wheezing, long exhalation, increased volume of lungs are determined. Heart: signs of CVF. Allergic rhinitis and (or) sinusitis or dermatitis. 

                  The clinical picture varies. Symptoms may be associated with URTIs, nocturnal or exercise-induced asthmatic symptoms, and status asthmaticus. Status asthmaticus, or an acute severe asthmatic episode that is resistant to appropriate outpatient therapy, is a medical emergency that requires aggressive hospital management. This may include admission to an ICU for the treatment of hypoxia, hypercarbia, and dehydration and possibly for assisted ventilation because of respiratory failure.

                   Physical findings vary with the absence or presence of an acute episode and its severity, as follows:

                    –Physical examination in the absence of an acute episode (eg, during an outpatient visit between acute episodes)

                   –The physical findings vary with the severity of the asthma. During an outpatient visit, it is not uncommon for a patient with mild asthma to have normal findings at physical examination. Patients with more severe asthma are likely to have signs of chronic respiratory distress and chronic hyperinflation.

                  Signs of atopy or allergic rhinitis, such as conjunctival congestion and inflammation, ocular shiners, a transverse crease on the nose due to constant rubbing associated with allergic rhinitis, and pale violaceous nasal mucosa due to allergic rhinitis, may be present.

                  The anteroposterior diameter of the chest may be increased because of hyperinflation. Hyperinflation may also cause an abdominal breathing pattern.

                 Lung examination may reveal prolongation of the expiratory phase, expiratory wheezing, coarse crackles, or unequal breath sounds.

Clubbing of the fingers is not a feature of straightforward asthma and indicates a need for more extensive evaluation and work-up to exclude other conditions, such as cystic fibrosis.

                            Barrel thorax

Allergic shiners. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)

Nose wrinkling of an allergic child. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)

Allergic salute. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990)

Transverse nasal crease in an allergic child. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)

"Rabbit nose" of allergic rhinitis. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)

Dark circles beneath the eyes of a child with allergic rhinitis. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)

Ocular allergy. (From Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990.)            

 Polymorphis erythema (Courtesy of Robert A. Silverman, M.D.)

Urticaria. (Courtesy of LM Pachter, M.D.)

                  Symptoms of asthma may include wheezing, coughing, and chest tightness, among others.

Wheezing: 

                     A musical, high-pitched, whistling sound produced by airflow turbulence is one of the most common symptoms. In the mildest form, wheezing is only end expiratory. As severity increases, the wheeze lasts throughout expiration. In a more severe asthmatic episode, wheezing is also present during inspiration. During a most severe episode, wheezing may be absent because of the severe limitation of airflow associated with airway narrowing and respiratory muscle fatigue.

                Asthma can occur without wheezing when obstruction involves predominantly the small airways. Thus, wheezing is not necessary for the diagnosis of asthma. Furthermore, wheezing can be associated with other causes of airway obstruction, such as cystic fibrosis and heart failure.

                Patients with vocal cord dysfunction have a predominantly inspiratory monophonic wheeze (different from the polyphonic wheeze in asthma), which is heard best over the laryngeal area in the neck. Patients with bronchomalacia and tracheomalacia also have a monophonic wheeze.