DIFFERENTIAL nDIAGNOSIS OF BRONCHIAL OBSTRUCTIVE SYNDROME IN CHILDREN.

EMERGENCY nASSISTANCE AT ASTHMATIC STATUS.

 

           Bronchial obstructive syndrome (BOS) nis a pathophysiological concept of violations of bronchial obstruction with a very nwide range of acute and chronic diseases.

         

 

          

        BOS – is a leading sign, which brings ntogether a group of acute, recurrent and chronic lung disease, but it is not aindependent nosological form and could not appear as a diagnosis. It should be nnoted that the BOS is not synonymous with bronchospasm, although in many cases, nbronchospasm is important, and sometimes a leading role in the genesis of the ndisease. Usually BOS is diagnosed in children of the first four years of life, nbut can be diagnosed in older age.

            In the genesis of bronchial nobstruction are different pathogenetic mechanisms, which can be divided into:

• functional or reversible (bronchospasm, inflammatory ninfiltration, edema,

        mucociliary insufficiency, nhypersecretion of viscous mucus)

• irreversible (congenital stenosis of the bronchi, their nobliteration, etc.).

            Peculiar features of the childreof the first three years of life have played the certain role in the ndevelopment of bronchial obstruction:

Þ   narrowness nof the bronchi and the entire respiratory system greatly increases

     aerodynamic nresistance. Thus, swelling of the bronchial mucosa by only 1mm

     causes aincrease in resistance to air flow in the trachea more than 50%.

Þ   softness nof cartilage bronchial tract

Þ   lack nof rigidity of the bone structure of the thorax, freely reacting indrawing of

     accommodating nplaces to increase the resistance in the airways

Þ   particular position and nthe structure of the diaphragm.

 

 

             BOS in children may be nsubstantially aggravated by structural features of bronchial wall, such as a nlarge number of goblet cells that produce mucus, and

increased viscosity of nbronchial secretions associated with high levels of cialic acid.

       nEarly childhood is characterized by the imperfection of immunological nmechanisms: significantly reduced the formation of interferon in the upper nrespiratory tract, serum immunoglobulin A, secretory nimmunoglobulin A, and reduced functional activity of T-immunity system.

                         

The nscheme of the basic mechanisms of bronchial obstruction.

1. nmaterial into bronchi (foreign body, mucous etc.)

2. nedema of bronchial mucous membranes (obstructive ndronchitis)

3. nretraction of bronchial muscles (bronchial asthma)

4. ncompression out of bronchus (mediastinum tumor, ndilatation of pulmonary artery

    at congenital nheart diseases)

 

                                       Etiology

 

                BOS usually is ninfectious-allergic nature. Among the viruses that most commonly cause BOS are nrespiratory syncytial virus (50%), then parainfluenza, rarely – influenza and nadenovirus. Recently, in the development of BOS big role is due to nintracellular pathogens. According to modern data, chlamydia and mycoplasma ninfection are determined in 20% of children with BOS.

According nto different authors, about 20-25% of bronchitis in children occur as an acute nobstructive bronchitis (AOB), which is significantly higher than in adults.

               Especially high frequency of AOB nis as a manifestation of acute respiratory infections (ARI) in infants. This is ndue to the fact that in the first half year of life 80% of the entire surface nof the lungs is small bronchi (diameter less than 2mm), whereas a child 6 years nold – already 20%. According to the Poiseul rule resistance of airways is ninversely proportional to their radius in the 4-th degree. Obstructive syndrome nof is the more probable in the distal lesion of the bronchi.

                                      Pathogenesis

                     

                Regulation of bronchial tone is ncontrolled by several physiological mechanisms, which include complex ninteractions receptor-cell component and mediators system. These include ncholinergic, adrenergic, neurohumoral regulatory system and, of course, the ndevelopment of inflammation. Interleukin-1 is the main mediator, initiating the nacute phase of inflammation. It activates a cascade of immune reactions that ncontribute to the exit in the peripheral blood of type 1 mediators (histamine, nserotonin and others).

               Histamine is released during aallergic reaction in the interaction of allergen with allergen IgE. In additioto histamine, a type 2 (eicosanoids) play an important role in the pathogenesis nof inflammatory mediators. Under the action of cyclooxygenase from arachidonic nacid there are synthesing prostaglandins, thromboxane and prostacyclin, while nunder the influence lipooxidaze – leukotrienes.

              The result is increased vascular npermeability, leading to swelling of the mucous membrane of the bronchi, nhypersecretion of viscous mucus, the development of bronchospasm. The maimechanism in the pathogenesis of bronchospasm is activation of cholinergic nnerve fibers, leading to increased production of acetylcholine and increasing nconcentrations of gualinatecyclase, which promotes the flow of calcium ions ninto smooth muscle cells, thereby stimulating of bronhoconstriction. nStimulation of α₂-adrenoceptor catecholamines, as well as aincreased concentration of cAMP decreases the manifestations of bronchospasm.

 

                                    Clinics of BOS

              The clinical picture of BOS ichildren is primarily determined by factors of bronhoconstriction. As noted nabove, in most cases BOS is associated with manifestations of acute respiratory nviral infection (acute obstructive bronchitis).  nSo body temperature is rised up nearly, catarrhal changes in the upper respiratory tract and violation of ngeneral condition of the child appear. The severity and the nature largely vary ndepending on what the agent has led to the disease. Signs expiratory breathing ndifficulties may occur as the first day of illness, and in the process of viral ninfection (3-5-day sickness). Gradually there is increasing the breathing nfrequency and duration of exhalation. Breathing becomes noisy and whistling, nwhich is due to the fact that with the development of hypersecretion, the naccumulation of secretions in the lumen of the bronchi due to shortness of nbreath and fever change viscosity of the secret – he “dries up”, nwhich leads to buzzing (low) and whistling (high) wheezes.

           The defeat of the bronchi is widespread, and therefore hard breathing with dry whistling nand buzzing wheezing are equally audible over the entire surface of the thorax. nRales may be heard at a distance. The younger the child, the more frequently he nhas, in addition to dry, the moist medium bubbling rales. If in the genesis of nbronchial obstruction a major role plays spastic component, it auscultative ndata over lungs is generally more diverse and labile during the day. With nincreasing dyspnea important role of supporting muscles becomes increasingly – nretraction of the intercostal spaces, epigastric and supraclavicular fossa, nbloating (voltage) of the nostrils. Often there are revealed perioral cyanosis, pallor of the skin, the child becomes restless, ntrying to adopt a sitting position, drawing on his hands.

              Respiratory failure more evident nthan the younger the child, but usually it is not more than II degree. Ophysical examination, in addition to scattered wheezes and hard breathing, nthere are the signs of lung swelling: narrowing boundaries of relative cardiac ndullness, boxed shade percussion tone. The inflation of the lungs is a result nof consequence wears small bronchial branches during expiration, which leads to nthe so-called ventilation emphysema. The volume of the lungs increases. The rib ncage is constantly in a state of inspiration, which increases the nanteroposterior size.

            Changes in peripheral blood ncorrespond to the nature of viral infection. Bacterial flora is rarely noverlapped – not more than 5%.

            Radiologically, in addition to nstrengthening bilateral lung pattern and expansion of the roots of the lungs nthere are revealed: lowness flattened dome of the diaphragm, increasing the ntransparency of lung fields, lengthening the lung fields, a horizontal narrangement of ribs on the radiograph, which mean the signs of swelling of the nlungs.

 

                             Diseases accompanied by BOS

 

              There are the following groups of ndiseases accompanied by BOS:

• nDiseases of the respiratory system – Infectious-inflammatory diseases (acute nconstrictive laryngotracheitis, bronchitis, bronchiolitis, pneumonia), allergic ndiseases (obstructive bronchitis, bronchial asthma), bronchopulmonary ndysplasia, malformation of bronchopulmonary system, tumors of the trachea and nbronchi.

• nForeign bodies of trachea, bronchus, esophagus.

• nDiseases of the aspiration genesis (aspiration or obstructive bronchitis) – ngastroesophageal reflux, tracheoesophageal fistula, malformations of the ngastrointestinal tract and diaphragmatic hernia.

• nDiseases of the cardiovascular system – Congenital and acquired (congenital nheart disease with hypertension, pulmonary circulation, vascular anomalies, ncongenital Non-rheumatic carditis, etc.).

• nDiseases of the central and peripheral nervous system (birth injury, myopathy, netc.).

• nHereditary anomalies of metabolism (cystic fibrosis, α1-antitrypsideficiency, mucopolysaccharidosis).

• nCongenital and acquired immunodeficiency states.

• nRare hereditary diseases.

• nOther states – Injuries and burns, poisoning, the effects of various physical and nchemical environmental factors, pressure on the trachea and bronchi of nextrapulmonary origin (tumor, venereal disease).

 

                       Diseases of the bronchopulmonary system

             The most frequently differential diagnosis of bronchial obstructiosyndrome in children is made among the diseases of the bronchopulmonary system.

 

BRONCOOBSTRUCTIVE SYNDROME AT PNEUMONIA

 

The edema of mucus nmembrane of bronchial tubes lies in the basis of syndrome, nhyperproductions of phlegm and, nin a less measure, bronchospasm, more frequent on a background of congenital or nacquired hyperreactivity of bronchial tubes are also important factor. This nsyndrome is identified at acute bronchopneumonia and is the reason of nrespiratory insufficiency on a bronchoobstructive type, which quite oftedetermines severity of the state and needs adequate oxygent therapy.

Clinic. Increase of ntemperature of body, trouble or oppression, crabbiness, pallor of skin with nperioral and acrocyanosis, unproductive cough, controlled from distance nwheezes, oral crepitation, shortness of breath, with prolonged one and hard nexhalation, drowning in chest of intervals between ribs, another areas of nchest.

Percussioreveals the tympanic sound with areas of short sound.

Auscultation: hard nbreathing with the prolonged exhalation, dissipated dry and moist wheezes, the nlocally loosened breathing with the isolated proof moist wheezes.

 

Help oprehospital stage

1.             nTo provide naccess of fresh air.

2.             nTo release nfrom squeezing clothes.

3.             nClean oral cavity and larynx from nmucus and  phlegma

4.             nOxygentherapy with clean moistened noxygen through a mask or oxygen

                      pillow.

5.             nInhalatioof dosed aerosol of Atroventi (ipratromium-bromide) 1-2

                  n    through nspenser.

           n6.     Inhalation of dosed aerosol nb_2-antagonists of quick actions (Salbutamoli,

        Ventolini, Berotec) 1-2 doses through spenser 20 minutes during hour.

        When it is impossible to make ninhalations- syrup, tablets of Salbutamoli

        or Terbutalini n(Bricaniliу)  to children upto 1 year – 1 mg 3 times, 3-6

        years – 2 mg 3 ntimes, 7-15 years – 2-3 mg 3 times; Clentuberoli

        (Spiropent) – 0,005-0,02  3 times; Broncholitini to  children upto 3 years–

        half ntea-spoon, 3-10 years  1 tea-spoon, elder n10 years is a 1 dessert-spoon

       3 times per ndays.

          7. nEuphyllini 3-5 mg/kg  – n2,4 % solution of Euphyllini in that  ndose 

                   nintravenously streamly on 10 ml of 10 %  glucose solution .

           8. n3 % solution of Prednisoloni 1-2 mg/kg  intramuscular.

           9. nHospitalization.

 

Help on a hospital stage

1. To provide access of fresh air.

2. To release from squeezing clothes.

3. nSucking with electrosucker mucus and phlegma from upper respiratory tracts.

4. Oxygenation therapy through a nasal catheter is nthe clean moistened oxygen during 20 minutes every 2 hours or 40 % oxygeconstantly.

5. Inhalation of dosed to the aerosol of Atroventi n(ipratromium-bromide) 1-2 dose through spenser.

6. Inhalation of dosed  aerosol b_2-antagonists of quick actions (Salbutamoli (Ventolini, Berotec) 1-2 doses through spenser 20 nminutes during hour. When it is impossible to make inhalations- syrup, tablets nof Salbutamoli or Terbutalini (Bricaniliу) children upto 1 year – 1 mg 3 times, 3-6 years – 2 mg 3 times, 7-15 nyears – 2-3 mg 3 times; Clentuberoli (Spiropent) – 0,005-0,02   3 times; Broncholitini to  children upto 3 years– half tea-spoon, 3-10 nyears- 1 tea-spoon, elder 10 years is a 1 dessert-spoon 3 times per days.

                                 

7.  3 % nsolution of Prednisoloni 1-2 mg/kg of  masses  nintravenously  streamly.

 8. 2,4 % solution of nEuphyllini 0,15 ml/kg of mass of  intravenously  in drops on

       10 % nglucose solution  10–15 nml/kg.

 9. nCocarboxilazae of a 5–10 mg/kg of mass on 5,0 ml of 10 n% Glucose solution

      intravenously  streamly.

 10. 5 % solution of sodium ascorbinati 2 ml/kg nof masses of   nintravenously  nstreamly

        on 5,0 ml of  10 % glucose solution .

 11. Panangini 0,1 ml/kgh of nmasses on 5,0 ml of 10 % Glucose solution

       intravenously  streamly.

 12.  Idefault of effect  ndrops intravenously introduction of Prednisoloni 2 – 3 mg/kg nof  the masses (Hydrocortisoni 10 – 15 nmg/kg) on 10 % Glucose solution  a 10 – n15 ml/kg of  mass.

 13. Mucolytic drugs: salt–alkaline inhalations; nLasolvani,Acetylcycteini  in inhalations, syrup, tablets; nBromhexini  in syrup, tablets; Mucaltini nin tablets.

 

         

 

 

 

Mucolytic inhalations

 14. Vibromassage of thorax in drainage position with nnext active aspiration of

       phlegm.

15. Alkaline ndrink: solution 1 % sodium bycarbonati per day to drink 10 – 12 ml/kg nof mass slightly.

                    

VIRAL nCROUP

 

Acute narrowing of larynx, conditioned by the ninflammatory edema of vocal cords and membranous space, hypersecretion of nglands, viral etiology, that is accompanied by the nhard breathing (croup).

 

Etiology: paraenfluenza I, ІІ type, flu I, rarely nRS–, adenovirus infection.

Children are ill from n6 months till 3 years old.

 

It is acute widespread ninfection-inflammatory disease with the phenomena of stenosis. In most cases it narises up under action of different respiratory viruses, mainly paraenfluenza, nmore frequent in age from 6 months to 3 years.

The most commopathogens are influenza viruses (56.8%), second in frequency space occupied by nparainfluenza viruses (20,1%), third – adenovirus n(16,7%),  at 6.4% of patients with acute laryngotracheitis there is a nmanifestation of a mixed viral infection.         

Mostly in the ndevelopment of acute laryngotracheitis a bacterial process is joined and may nchange the clinical picture.

Laryngoscopic picture nwith stenosing laryngotracheitis is characterized by the formation of rollers nunder the vocal ligaments and the presence of mucous-purulent discharge ithe tracheobronchial tree. Some authors, except edematous form of stenotic nlaryngotracheitis, allocate purulent, fibrinous, necrotic, and other forms. nAfter the obstruction at the level of the larynx there is a violation of ndrainage function of tracheobronchial tree, resulting in the appearance of ninflammation in the lower respiratory tract, including lung tissue.

 

Stenosis is a result nof mucus and submucous tissue edema of larynx below vocal ligaments, naccumulation of mucus, reflex spasm of muscles.

 

 

 

Schematic stages of nthe introduction of a laryngoscope with the direct laryngoscopy and the ncorresponding laryngoscopic picture – the end of a laryngoscope blade presses nthe epiglottis to the root of the tongue: 1 – aryepiglottic cartilage, 2 – ninteraryepiglottic hollow, 3 – vocal cords, 4 – folds of the laryngeal nvestibule.

 

    

 

 

 

Endoscopy image of nlarynx

Aquied undercord nstenosis

(narrowing nof respiratory tract)

 

 

The thickness of nrespiratory tracts is decreased, resistance of air grows. Inflammation, edema, nspasm, presence of inflammatory exudation of respiratory tracts are the basic nlinks of pathogenesis, which result in violation of breathing, hypoxia, nhypercapnia. An inflammatory process can spread on a trachea, bronchial tubes.

Clinical nclassification of acute laryngotracheitis:

I. Type of respiratory viral infection: 1) influenza, parainfluenza, nadenovirus infection, etc., and 2) ARVI (is specified in the impossibility of nclinical interpretation and the absence of express-diagnostics).

II. Degrees of laryngeal stenosis: 1) compensation, 2) incomplete ncompensation, 3) decompensation, 4) terminal.

 

 

Clinic. The characteristic is triad of symptoms: the nchange of voice, rough, “barking” cough, stenotic breathing. More frequent nstenosis laryngitis develops suddenly among night. There are 4 degrees of nlarynx stenosis.

 

I ndegree (compensated stenosis): hoarse of voice, rough “barking” cough, ncompensated hyperventilation of lungs, рО₂ – within the limits of nnorm.

 

The ІІ degree (subcompensated nstenosis): the child is excited, voice getting hoarse, nrough, cough increases, the inciter shortness of breath appears. A skin is  moist, pallor, ncyanosis of perioral triangle. Breathing is with participation of auxiliary nmuscles. Hyperventilation of lungs gradually changes on hypoventilation. nConsiderable tachycardia, рО₂ is not reduced. Metabolic acidosis develops.

 

The ІІІ degree (decompensated nform of stenosis) is the severe state. A child is excited. There are loosened nvoice, expressed inciter shortness of breath (inspiration is prolonged with nstenotic noise). Breathing with participation of all auxiliary muscles. nFrequent “barking” unproductive cough. A skin is pale, covered by a cold sweat, nconsiderable cyanosis of nasooral triangle, lips, tongue, nail nphalanges. Tones of heart are deaf, tachycardia, decreased arterial preassure, na pulse is frequent, weak. In lungs there is decreased breathing, superficial, nis badly listened, sternum is down in. рО₂ of arterial blood is reduced, рСО₂ is npromoted, mixed acidosis develops (metabolic and respiratory).

 

The nІV degree (asphyxia): a child nis in the extraordinarily severe condition, without consciousness. Cyanosis of nskin, a pallor develops later. Breathing is superficial, frequent, with the nquick stops with next deep inspiration. At auscultation the breathing is not  listened. Tones nof heart are deaf, decreased arterial preassure, a pulse is threadlike, later bradycardia, arrhythmia develop, which  precede to the stop of heart. In a nblood рСО₂considerably grows (to 100 ml Hg and higher) and рО₂ nconsiderably goes down (to 40 ml Hg.). The child dies from the asphyxia.

 

                 Differential diagnosis of real and false croup

n

Real croup	False croup
Acute start	Permanent start
Febril high t°	Subfebril t°
Catarrhal sings are expressed	Catarrhal sings are absent
Skin is moist, cyanotic	Skin is “toxic”, pale
Hyperemia, edema of pharynx	Grey-dirty tapes o tonsils after their scopes
Voice is hoarse	Aphonia
Edema of  subcutaneous tissue is absent	Edema of  subcutaneous tissue of neck
Absence of signs of palate paresis	Effluence of liquid through a nose

 

Primary naim of treatment is to pick up thread passage of respiratory tracts and remove nhypoxia.

 

                   Help non prehospital stage

The volume of medical nmanipulations depends on the degree of stenosis

severity.

I degree:

1.             nDistracting nprocedures:

       –warm tender baths, it is possible with nmustard

             –mustard plasters on a thorax, on an area of laryngs

             –at allergy to mustard semialcoholic hot compress on a thorax,

              on nthe area of neck

              –warm alkaline drink: mineral water, tea with 2 %  solution of soda,

                 warm nmilk

2.             nOxygentherapy: n

                     –warm, moistened air

   –soda inhalations.

3.             nIchildren with the allergic reactions – Suprastin orally, in a dose 2 mg

                      per nthe kg of mass; from 2 years 1 tea-spoon of Claritini in syrup.

4.             nHospitalizatioin the diagnostic or infectious unit.

 

ІІ degree.

1.             nIntramuscular n2 % solution of Suprastini 2 mg per the kg of mass.

2.             nIexcitation – 0,5 % solution of Seduxeni (Sibasoni, Relanium) in a

                     ndose 0,3-0,5 mg per the kg of mass nintramuscular, or 20 % solution

                     nof  Oxybutirati nsodium in a dose 50 mg per the kg of mass

                      intramuscular.

3.             nDistracting nprocedures:

        – warm tender nbaths, it is possible with mustard;

        – mustard nplasters on a thorax, on an area of laryngs;

              – at nallergy to mustard semialcoholic hot compress on a thorax, on the

                   area nof neck.

4.                nWarm nalkaline drink: mineral water, tea with 2 % soda solution, warm

                     nmilk.

5.                nOxygentherapy: n

                    – warm, nmoistened air;

  – soda inhalations.

6.             nHospitalizatioin the intensive unit or chamber of intensive therapy for diagnostic or ninfectious separation.

 

ІІІ degree.

1.             nSucking of nmucus from a mouth cavity, respiratory tracts;

2.             nOxygentherapy: nwarm, moistened air through a mask;

3.             n0,5 % nsolution of Seduxeni (Sibasoni, Relanium) in a dose 0,3-0,5 mg

                     nper the kg of mass intramuscular, or 20 % nsolution of Oxybutirati

                     nsodium in a dose 50 mg per the kg of mass nintramuscular;

4.             nHydrocortisoni nintramuscular in a dose 5 mg per the kg of mass or 3 %

                     nsolution of Prednisoloni intravenously in a ndose 1 mg/kg of mass.

5.             nDistracting nprocedures:

           – mustard nplasters on a thorax, on an area of laryngs;

           – at nallergy to mustard semialcoholic hot compress on a thorax,

              on the narea of neck.

6.             nOxygentherapy nthrough a mask.

7.             nHospitalizatioin the intensive unit of child’s hospital.

 

ІV degree.

1.             nSucking of nmucus from the cavity of mouth, respiratory tracts.

2.             nOxygentherapy nthrough a mask, aerotherapy with the warm moistened

                     nair.

3.             nIntravenously nstreamly 3 % solution of Prednisoloni in a dose 1-2 mg

                     nper the kg of mass of body.

4.             nIntravenously nstreamly 10 % solution of Calcium gluconatis in a dose 1

                    nml per the year of life.

5.             nAt ndeparture on the call of the specialized brigade and equipped

                       ambulance nthe intubation of patient.

6.             nHospitalizatioin the intensive unit of child’s hospital.

 

                             Help non a hospital stage

Permanent observatioof a patient who is hospitalized, the unit must be equipped by the inhalators nof the «fog» type, ІP-2 and others, by oxygen tents, in which the proper nmicroclimate is created (temperature 30 ⁰C, moisture 100 %, 40-50 % oxygen).

I degree.

1.         nInhalations nby the moistened 40 % oxygen, oxygen is possible to skip

                    nthrough Bobrov apparatus, through the water extract of camomile, clary,

                    ninfusion of  eucalyptus, 2 % nalkaline solution. Treatment in a oxygen tent

                    n2-3 times per day.

                n

 

 

Oxygen tent for babies and young children (up to 3 nyears) is used in maternity hospitals and children’s hospitals for oxygetherapy procedures.

 

  nSalt-alkaline inhalations or inhalations of such composition:

           – 5 % solution of ascorbic acid – 5,0;

           – 5 % solution of Ephedrine  – 1,0;

                 n–0,1 % solution of Adrenalin  – n1,0;

                 n–Hydrocortisoni 25 mg;

                 n–3% solution of sodium hydrocarbonatis 6,0.

On inhalation – 4 ml nof solution. In the first 2 days inhalations are done 4

times per day, on 3th nday – 3 times, on 4-6th days – 1-2 times per day.

2.         nDistracting ntherapy: mustard plasters on a thorax, tender baths, ozocerite

                    nor paraphine “knee-boots”, warm drink.

3.         nSucking of nmucus.

 

ІІ degree.

1.             nAt the nprotracted stenosis there is direct laryngoscopy for diagnostics of

                       inflammatory process, nsucking of mucus (clearning of tracheobronchial

                       tree and larynx);

2.             nProtracted ninhalations of warm, moistened air, stream through mask or

                      under framework which ncovers a bed, in which a patient is (moisture to

                       90-100 %, temperature to n26-30 0С)  for 3-4 hours; noxygen tent.

                n

                n

Oxygen therapy through a mask.

3.             nInhalations nwith the medicine mixture:

1)            n5 % nsolution of Ephedrine – 0,5 (1) ml,   nHydrocortisone 12,5 (25) mg,

                 1 % Dimedroli solution – 0,5 n(1) ml, 0,5 % solution of sodium  nchloride

                 – 3-4 ml (in handles there nare  the indicated doses for childremore

                    senior than 1 year old),

2)            n antiedema mixture: 5 % solution of nEphedrine  1,0; 0,1 % solution of

                   Adrenalini 1,0; 0,1 % nsolution of sulfate Atropine  – 0,5; 1 % nsolution

                   of Dimedroli – 1,0; 2,5 % nsolution of Pipolpheni 1,0; Hydrocortisoni

                  25 mg; Hymotripsini 2 mg in 1 nml of liquids; 5 % solution of ascorbic

                  acid – 5,0. On one inhalation 4 ml nof mixtures are used.

                n

Stream ninhalator

4.             nAt the nexcitation 20 % solution of  Oxybutiratis nsodium  intravenously

                      streamly slowly in a dose n50 mg per the kg of mass.

5.             n2,4 % nsolution of Euphyllini intravenously streamly slowly in a dose

                   n1 ml per the year of life on 10 % glucose solution.

6.             nIntravenously nin drops 10 % Glucose solution , 0,9 % solution of sodium

                    n chloride (in the ratio 3:1) + 5 % nsolution of ascorbic acid – 1-2 ml,

                    nCocarboxilazae 5 mg per the kg of mass; 15-20 drops in 1 minute.

7.             nDistracting ntherapy: mustard plasters on a thorax, tender baths, ozocerite

                      or paraphine n“knee-boots”.

 

ІІІ degree.

            1.  nHospitalization in intensive unit.

            n2.   Inhalation therapy in oxygetent, 4-6 inhalations per day.

            n3. 20 % solution of Oxybutiratis sodium  nintravenously streamly slowly in a

            ndose 50 mg per   the kg of mass; nin 3-4 hours – 0,25 % solution of

            nDroperidoli 0,3-0,5 ml/kg of mass.

           4. nDirect laryngoscopy for diagnostics of inflammatory process, clearning

             nof larynx, respiratory tract.

           5. 3 % solution of Prednisoloni nintravenously streamly in a dose 2-3 mg per

              nthe kg of mass.

           6. nInhalations to the aerosol: 0,1 % solution of Adrenalini 0,5-1 ml per

             n3 ml of isotonic solution of sodium chloride together with oxygen

             nduring 5-10 minutes; with a antiedema mixture.

    

      

Dummy- inhalator that nis compatible with standard sockets inhalator supply gas or mixed medication to nthe nose of the child. Dummy is reusable, capable of being sterilized by nstandard autoclaving or disinfectants.

 

          8. n2,4 % solution of Euphyllini intravenously streamly nslowly in a dose 1 ml per the year of life on 5-10 ml of  0,9 % isotonic solution.

           9. nIntravenously in  drops (20-25 drops for na minute) 10 % solution of Glucose, 10-20 % solution of Albumini or similar ngroup Plasma in a dose 5-10 ml on the kg of mass of body; Reopoliglucini in a ndose 10 ml on the kg of mass of body, correlation of glucose to the salt and ncolloid solutions 2:1. Common amount of liquid is a 30-50 ml/kg of mass daily.

           n10. 4 % solution of Hydrocortisoni 4-8 ml per the kg of mass nintravenously in  drops, nin 2 injections under the control of acid- alkaloid balance.

            n11. 10 % solution of Calcium gluconatis intravenously streamly slowly ia dose 1 ml per the year of life.

            n12. Antibiotics:

1)    nCephalosporins: nDuracef (Cefadroxil), suspensia 50 mg per the kg of mass per  day for 2 receptions in interval 12 hours; nKefsoli 75-100 mg/kg of  the masses per nday for 2 receptions intramuscular;

2)    nMacrolides: nsuspensia of Macropeni  na 50 mg/kg of  mass per day nin 2 receptions, summamed a 10 mg/kg of  nmass per  day.

3)    n            13. Indication to intubation: nhypoxemia (рО₂ below 50mm Hg) with concentration of oxygen during inspiratiohigher 50 %; hypercapnia, acidosis( рСО₂ nhigher than  55 mm Hg, рН less than 7,35); encreasing of  languor, somnolence.

IV degree.

1.             nIntubatiowith soon artificial breathing. Advantage it to give nasotracheal intubation, nas to more sparing and simple method.

2.             nClearning nof respiratory tract with the use of warm isotonic solution with nhydrocortisoni, euphyllini; 1 % by solution of hydrocarbonatis,

                    n   antibiotics nof wide-spread action (a few times per days);

3.             nOxygentherapy nwith moistened oxygen.

  

 

Ventilator Vent201, created by the most modertechnologies, provides high quality ventilation and provides an easy transitiofrom noninvasive to invasive ventilation.

 

Ventilation, neuro-controlled respiratory support n(NAVA) Servo-I (Maquet). Allows you to maintain respiratory activity of the npatient using his oweuro impulses.

4.             n3 % nsolution of prednisoloni intravenously streamly in a dose of  3-5 mg

                      per the kg of mass or nhydrocortisoni intravenously in drops (15-30

                      drops in 1 minute) in a ndose 15-20 mg per the kg of mass on 100-150

                      ml 0,9 % sodium chloride nsolution.

5.             nIntravenously nin drops 10 % solution of glucose, 0,9 % sodium chloride

                      solution, Reopoliglucini nin a dose of 10 ml per  the kg of mass.

                     nCorrelation of glucose and salt solutions to the children upto 1 year nold

                     nis 3:1 or 4:1, from 1 to 2 – 1:1. Fresh-frozen plasma in a dose 10 ml nper

                     nthe kg of mass. Common amount of liquid is 40-50 ml per kg of mass

                     ndaily. To conduct infusion therapy 2 times per day.

6.             nWith   infusion solutions intravenously enter 5 % nsolution of ascorbic

                     nacid 1-2 ml, 10 % solution of chloride calcium  1 ml per the year of life,

                n     Cocarboxilazae in a dose nof  5 ml per  the kg of mass.

7.             nSymptomatic ntherapy.

8.             nDynamic nobservation of paediatrician, reanimatologist, otolaryngologist.

9.      Determination of рО₂, рСО₂, nЕCG.

 

In all stages of stenosis must be indicated:

1.             nAntienfluenza ngamma-globulini in 1 dose till 1 year; 2 doses till 3 years,                                               n3 doses to the children more senior then 3 years.

2.             nObservatiofor the exception of diphtheria (stroke from a nose and                  pharynx).

3.             nConsultatioof otolaryngologist.

4.             nAt saving nof swallowing- warm alkaline drink (mineral water, flora tea               with 2 % soda solution ), milk.

 

ACUTE nOBSTRUCTIVE BRONCHITIS

 

In the basis of syndrome is violation of the bronchial npassage, conditioned by the diffuse inflammatory edema of mucus, hypersecretioand accumulation of mucous and purulent phegma in bronchial tubes, transitory nreflex spasm of smooth musculature.

 

                 Until the 70’s, the last ncentury, the term “obstructive bronchitis and its analogs (asthmatic nbronchitis, spastic bronchitis, etc.) were widely used by pediatricians. nHowever, in the early 70’s a series of epidemiological studies were performed, nwhich showed that distinguish obstructive bronchitis and asthma in the general npediatric practice is almost impossible. Thus, equal sign between these states nwas put. This approach in older children has largely justified itself, as would nsave many patients from antibiotic therapy. But in younger children the problem nis more complicated. It was established that cromoglycate in these patients is nnot effective enough or not effective at all. Inhaled bronchodilators such as nsalbutamol, are ineffective enough or not effective at all at wheezing in childreof the first three years of life. Information regarding the effectiveness of ninhaled steroids for acute or chronic bronchiolitis was contradictory.

               In addition, numerous studies iour country and abroad have shown that the outcomes of obstructive bronchitis nin general are favourable. 54% of children with repeated episodes of nobstructive bronchitis stopped hurting after four years, and another 37% of – nat a later age, thus recovering is more than 90% of patients. In addition, the npresence of obstructive syndrome in the first three years of life caot be nconsidered as a factor predisposing to the appearance of asthma in the future. nThat is, it became clear that the mechanism of development of wheezing iinfants, other than for the older children, and the main role is played not nhyper reactivity in bronchial mucosa and muscle spasm and tone of the bronchial nwall and edema of bronchial mucosa. This reflects the fact that n”wheezing” in young children is a consequence of various causes, nincluding abnormalities of the respiratory system and inflammatory processes of nother etiologies.

 

Clinics: subfebril ntemperature, trouble, crabbiness of child, cyanosis of lips, nasolips triangle, nacrocyanosis. Dyspnea, noisy, with the prolonged inspiration and  distance wheezes. Downing in of interrib nintervals, supraclavia areas, jugular pit.  nUnproductive coughing. A thorax is emphysematous, at percussion above nlungs -box sound, аt nauscultation- breathing is hard, with the prolonged inspiration and dry and different nmoist wheezes, character of which is changed after a cough. Таchycardia. A liver is often enlarged. In the ngeneral blood analysis there is not substantial changes or insignificant nneutrophyls leucocytosis.

 

                

                                           Barrel thorax

Diagnostic ncriteria of acute obstructive bronchitis in children

  – Long nwhistling breath, which is audible at a distance                        

– Inflated thorax when viewed from (horizontal nplacement

    ribs) participated nin the act of breathing support muscles,

   retraction of nthe intercostal spaces, signs of respiratory

    failure

– Dry cough, paroxysmal, prolonged and at the end of nthe first

   week passes nin the moist

– Percussion determined bandbox pulmonary sound

– Auscultation: hard breathing, exhaling is prolonged, n

   large amount nof dry whistling rales. There may be coarse

   bubbling low nsound rales

– On the chest radiograph is observed decreased lung

   pattern in the nlateral regions of the lungs, and increased in the medial

  (hiddeemphysema).

 

On the X-ray of thorax organs – the strengthening of npulmonary pattern, areas of promoted pneumatization without of infiltratiochanges in lungs.

 

     

 

Radiographs nof the chest in front projection with AOB: total marked bilateral increase the ntransparency of lung fields, depletion of vascular pattern on the periphery nwith its increasing in the central parts, the expansion of the roots of the nlungs and flattening of the diaphragm.

 

              Differential diagnosis of obstructive bronchitis and pneumonia

 

n

Symptoms	Obstructive bronchitis	Pneumonia
Temperature	Subfebril	Hyperthermia
Intoxication	Absent or slight	Expressed
Dyspnea	+	+
Dry whistling rales	+	–
Local moist rales	–	+
Percussion sound	Bandbox	Dull
X-ray	The strengthening of pulmonary pattern	Local (segmental, lobe, focal) infiltrates

 

 

    nDifferential diagnosis of bronchial asthma and obstructive nbronchitis 

 

n

Symptoms	Bronchial asthma	Obstructive bronchitis
Allergologic anamnesis	Positive	Sometimes positive
Start of illness Catarrhal sings of ARVI	Attack of dyspnea with or without ARVI	Gradual increasing of symptoms
Temperature	Normal, sometimes increased	Everytimes increased
Course of disease	Repeating attack of dyspnea	Frequency of obstructive episodes decreases, recovery is possible
Ig E	Increased	Normal
Eosynophylia in blood	Present	Absent

 

 

Help on prehospital stage.

1.             nTo provide access of fresh air.

2.             nTo release from squeezing clothes.

3.             nSuccing with electrosuccer mucus and phlegma from nupper

                     respiratory tracts.

4.             nOxygentherapy with  nclean moistened oxygen through a mask.

5.             nBroncholytin for  children upto 3 years– harf of  tea-spoon, 3-10 years

                    a 1 tea-spoon, more senior nthan 10 years  a 1 dessert-spoon 3 times nper

                   day or Solutani 5-10 ndrops 3 times per  day.

6.             nEuphyllini in  ndose of a 3-5 mg per kg of  mass norally or 24 % Euphyllini

                             solutiointramuscular.          

7.             nSalt-alkaline inhalation.

8.             nIn default of effect – hospitalization.

 

Help on  hospital stage.

            1. Succing with electrosuccer mucus nand phlegma from upper respiratory

               tracts.

            2. Oxygentherapy through the nnasal catheter with 40 % moistened oxygen

               constantly.

 

 

               

Nasal catheters for oxygenotherapy

 

            3. Inhalations of nbroncholitic mixture: Euphyllini – 0,3, ephedrine  – 0,2,

               novocaine – 0,25, water – 50,0 мл. On inhalation 3–5 ml, before inhalation

               to add 1,0 ml of  5 % sodium ascorbinati solution .

            4. Mucolytic drugs: nsalt-alkaline inhalations; Acetylcysteini or Lasolvani in

               inhalations, syrup, tablets; nMucaltini in tablets, extract of altey.        

            5. Vibromassage of  thorax in drainage position with next active naspiration

                of phlegma.

           6.  n2,4 % solution of Euphyllini 3-5 mg/kg of  nmass of intravenously

                 in drops on isotonic nsolution of chloride sodium  10-15 ml/kg nof mass.

          7. 5 % solution of sodium ascorbinati 0,2 nmg/kg of the masses intravenously

               streamly on 5 ml of  10 % glucose solution .

          8. Cocarboxylazae 5-8 mg/kg of mass nof intravenously streamly on 5 ml of 

              10 % glucose solution.

          9. In default of effect from previous therapy nPrednisoloni 1–2 mg/kg of the

              masses (or Hydrocortisoni 5 mg/kg nof  mass) intravenously streamly on

             5 ml of  10 % glucose solution.

          10. Alkaline drink: 1 % solution of nsodium bicarbonates 10-15 ml/kg of 

              mass  per day.

 

ACUTE nBRONCHIOLITIS

 

Development of total nobstruction of respiratory tracts lies in basis of syndrome, which is  conditioned with the expressed hypersecretioof phlegma, with the edema and swelling of mucus of  bronchial tubes and bronchiols and, in a less nmeasure, bronchospasm in  the children of nthe first year of life on a background of viral, more frequent nrespiratory-syncitial infections.

 

Criteria of diagnosis of bronchiolitis:

1. nPresence of the catarrhal phenomena n(rhynopharyngitis, cough).

2. nTemperature of body – subfebrile, rarely 38^oС. n

3. Expressed nsigns of respiratory insufficiency:  nshortness of breathing, blowing nostrils, cyanosis of nasolabial ntriangle, participation of auxiliary musculature.

4. Violation of the bronchial passage: thorax is nemphysematosis; horizontal position of ribs, flat position of diaphragm.

5.Bandbox sound at percussion.

6. Auscultation: hard  nbreathing  with prolonged inspiration, moist wheezes, on outbreathing – dry, whistling.

7. Cardiovascular syndrome – tachycardia, weakening of tones.

8. X-ray– sharp swelling of lungs tissue, increased nbroncho-vascular pattern, without infiltrative shades; sometimes atelectasis.

 

 

 

Clinic. Syndrome of airway obstruction lies at the basis nof acute bronchiolitis, which is more typical for children of the first six nmonths of life. In acute bronchiolitis body temperature is subfebrile or nnormal, respiratory failure progresses gradually. Signs of intoxication are ninsignificant. Characteristic features are perioral or acrocyanosis, dry cough, na large number of small moist rales on both sides – “wet” lung and a nsmall number of dry wheezes. 

In severe cases ndyspnea has predominantly expiratory character, groaning breath, tension and nswelling of nostrils, participation in the act of breathing supporting muscles, ngeneral cyanosis of the skin. Nonproductive cough, frequently emphysematous nswelling of the chest are present. Above the lungs percussion sounds are nbandbox, throughout the lungs a large number of small bubbling and wet ncrepitative wheezing. There are tachycardia, increased liver,  may be attacks of apnea, hypoxic seizures, ndehydration.

X-ray examinatioshows the symmetric strengthening of pulmonary pattern of  both sides, increase of transparency of npulmonary tissue, absence of infiltratative shades. In the blood test the nappropriate changes are absent.

 

Help oprehospital stage.

1.             nTo nrelease from clothes.

2.             nTo give nthe promoted position of body to the child.

3.             nBy a nrubber bulb or gauze clean the  nasal ncavity, mouth and pharynx

                     nfrom mucus and phlegma.

4.             nTo provide naccess of fresh air.

5.             nOxygenatiowith clean moistened oxygen through a mask.

6.             nEuphyllini nin dose of 3-5 mg/kg of mass -24 % solution intramuscular.

7.             n3 % nsolution of Prednisoloni 1-2 mg/kg of  nthe masses  for 

                     ndose intramuscular

8.             nSalt-alkaline ninhalation.

9.             nUrgent nhospitalization.

 

Help non  hospital stage.

1.             nTo nrelease respiratory tracts from mucus and phlegma with the help

                       of electrosuccer.

                            

 

2.             nOxygentherapy nwith  moistened warm 40 %  oxygen through a nasal

                    ncatheter or mask 3-5litres per 1 minute.

3.             nInhalatioof broncholytic mixture: Euphillini – 0,3, ephedrine – 0,2,

                     nnovocaine – 0,25, water – 50,0 ml. On inhalation 3-5 ml, before

                    ninhalation to add 1,0 ml of  5 % nsolution of sodium ascorbinati.

4.             nInhalations nof mucolytic drugs – 2 % solution of sodium hydrocarbonatis

                     n3-5 ml, Acetylcysteini, Bisolvoni, Lasolvani  2-3 ml on inhalation with

                    nnext aspiration of phlegma.

5.             n2,4 % nsolution of Euphyllin 3-5 mg/kg of mass on 10 % glucose solution

                      10 ml/kg of mass of nintravenously slowly.

6.             n3 % nsolution of Prednisoloni 1-2 mg/kg of the masses, one dose

                        intravenously streamly non 10 %  glucose solution 10 ml.

7.             n5 % nsolution of sodium ascorbinati 0,2 ml/kg of the masses

                    nof intravenously streamly on 5 ml of  n10 % glucose solution .

8.             nCocarboxylazae n5-8 mg/kg of  mass of intravenously nstreamly

                     non 5 ml of  10 % glucose solutio.

9.             nAlkaline drink: n1 % solution of sodium hydrocarbonatis  n10-15 ml/kg

                     nof mass per day.

10.        nVibratiomassage of thorax in drainage position.

11.        nIn default nof effect and enlargement of respiratory insufficiency – 

                     nclearing of bronchial tree by bronchoscope,  artificial ventilation.

                 

                          Sonotherapy at nbronchiolitis

                              BRONCHOPULMONARY DYSPLASIA(BPD)

                   In recent years increasingly nrelevant bronchopulmonary dysplasia (BPD).

              BPD is acquired chronic nobstructive pulmonary disease that develops as a result of respiratory distress nsyndrome of neonates and / or artificial ventilation (AVL) with high nconcentrations of oxygen, accompanied by hypoxemia, altered reactivity of the nbronchi with hypersensitivity of airways, and typical radiological changes.

              In the etiology of BPD there are nmany factors: the impact of oxygen in high concentrations, mechanical nventilation, pulmonary edema, left to right shunt at patent ductus arteriosus, nrecurrent bacterial pneumonia, hereditary predisposition, hypovitaminosis A and nE.

 

                             Pathological Anatomy and Physiology

 

                    According to the results of postmortem nstudies, there are 4 stages of BPD, which are similar to roengenologic nfindings. In the first three days of life (I stage), there is a typical nrespiratory distress syndrome. In the following days the first week of life (II nstage) there are destruction of cells of the alveolar epithelium and capillary nendothelium, interstitial edema and perivascular space, necrosis of the nbronchioles, squamous metaplasia, hypertrophy of smooth muscle cells of the ndisappearance of ciliated epithelium. In the II-III week (III stage) there is nincreasing of the number of macrophages and plasma cells and fibroblasts. nProcess damage the bronchial tubes of different orders, which in severe cases nleads to obliterative  bronchiolitis. Ithe following week atelectasis zones with interstitial and peribronchial nfibrosis in conjunction with areas of emphysema (IV stage) are revealed. In the nwalls of the alveoli there is increasing of the number of reticular, collagen, nelastic fibers, which structure is disrupted.

                 Naturally pulmonary emphysema ndevelops caused by three mechanisms: 1) scars that appear due to hyperextensioof nonfibroid lung; 2) violation of the multiplication of alveoli in some areas n(atrophic form of emphysema); 3) destruction as a result of the inflammatioand destruction of the walls of the alveoli and capillaries. Structural changes nof the pulmonary arteries include intimal proliferation, smooth muscle nhypertrophy, the proliferation of smooth muscle on the distal parts of vessels, nthickening and fibrosis of the adventitia, the decreasing of diameter of the narteries.

 

             In diagnosing BPD anamnestic data nare important:

·        nprematurity

·        nbirth weight less than 1500g

·        nRDS in the first hours of life

·        nALV with rigid parameters for more nthan 6 days

·        noxygen dependance at least 1 month.

 

                                  Clinic:

            Specific clinical manifestations of nBPD are absent. The clinical picture of BPD symptoms is presented with chronic nrespiratory failure (tachypnea to 80-100 per minute, cyanosis, emphysema, rib nretraction, persistent physical examination changes in the form of an elongated nexhalation, dry wheezing, moist small bubbling rales, stridor is possible) ipreterm infants who are dependent on high concentrations of oxygen in inhaled nair and mechanical ventilation for a longer or shorter time.

           Resistant respiratory failure ndevelops after the initial improvement under AVl. This dependence on oxygen and nmechanical ventilation may be manifested in different ways.

           The diagnosis of BPD brings together na wide range of clinical manifestations and changes on the radiograph. In mild ncases may be observed only the impossibility of reducing the oxygeconcentration and the parameters of artificial ventilation for 1-2 weeks, nlengthening the period of recovery from respiratory failure. In severe cases ithe background of AVL hypoxemia, hypercapnia remain, “remove” a child nfrom a ventilator is impossible within a few months, reintubations are ncharacteriatic. Typically, the suspicion of BPD occur when the child needed nmechanical ventilation, especially with positive end-expiratory pressure, for nmore than 1 week. Cough, persistent symptoms of bronchial obstruction syndrome ipatients are preserved  on already nspontaneous respiration.

           Further, after the neonatal period, ncourse of BPD is wavy, depending on the degree of morphological and functional ndisorders. The majority of patients showed a slow but clear improvement and nnormalization of the state in 6-12 months, but in some patients violations npersist for a long time. According to observations GM Dementieva et al. (1997) nat 16-20% of children discharged from office for prematurity, pathological nchanges in the lungs retained and in older age – for 1-4 years of life, and 4% nof patients BPD in the future lead to disability. Recovery in children with BPD nmay be due to the fact that along with the fibro-proliferative processes in the nlungs of preterm there is occurring regenerative process and continuing growth nand development of the lungs.

         Examination reveals the cough and npersistent physical examination changes, the increasing of obstructive ndisorders at virus infection, the symptoms of latent respiratory insufficiency ndetected by the load – sucking, moving, crying, while often develop pulmonary nheart at an early age, neurological disorders, retarded physical development. nThe final diagnosis is established after the radiographic examination with nsigns of fibrosis in the form of deformation and strengthening of local lung npattern or a light disguise lung fields in middle medium sections, alternating nwith areas of swelling of lung tissue, primarily in low lateral areas ichildren older than 1 month.

Roentgenography of child 5 mths with BPD n 

           Activities nfor the prevention of BPD include:

1. nPharmacological acceleration of lung maturation: prenatal prevention of RDS naccelerates the maturation of surfactant synthesis and is one of effective nmethods of reducing the frequency and severity of BPD. Birth of a baby without nthe RDS  gives possible to avoid nmechanical ventilation, and consequently, the mechanical (positive pressure) nand chemical (oxygen) injury of the lungs. One of the most common methods of prenatal nprevention of RDS is the GCS therapy, which stimulates the synthesis of nsurfactant in the lungs of the fetus.

2. Rational netiopathogenic therapy of RDS: in preterm infants it involves the use of nexogenous surfactant preparations that can achieve the reduction of severity nand reducing the duration of the disease and, consequently, the duration of nmechanical ventilation and oxygen therapy in general.

3. Selectioof the optimal level of respiratory support of  nchild: currently there is no doubt that the early onset of respiratory ncare can reduce its duration and limit the softer options like the pressure and nthe oxygen content. Early spontaneous respiration under constant positive npressure of (SRCPP) makes it possible to limit the scope of respiratory care, nstop the progression of RDS and avoid the need for mechanical ventilation.

               At mechanical ventilation it nshould be strive to limit the minimal sufficient level of peak pressure and nminimal sufficient concentration of oxygen. A special problem is a return the nchild from mechanical ventilation to spontaneous respiration. This is a long nprocess, involving a slow decrease in ventilatory parameters, transfer the nchild to SRCPP through endotracheal tube, and then – through a nasal cannula.

4. Proper nmaintenance of water balance and energy supplementation: control of water nbalance is reduced to restrict fluids to 90% of fluid consumption. Excessive nhydration leads to the pulmonary edema and disorders of gas exchange.

              Already in the early stages of nBPD childreeed increased energy supply. Parenteral nutrition in the first ndays of life is intended to prevent catabolic processes. The full parenteral nproviding of proteins, carbohydrates, fats, vitamins and micro elements is nimportant to limit further damage to the lungs and create conditions for their nrepair.

              In children with already nestablished BPD in terms of water balance, their treatment has a number of nperculiarities. Children with BPD have little resistant to the normal amount of nfluid and tend to accumulate it in their lungs. They have  problems with nutrition, manifested in aimbalance between the demand of food and limitation of fluid. Often grows nretardation occurs, so callories  should nbe increased, due to immaturity, growth need, increased work of breathing, high nlevels of metabolism (the additional cost of the energy supply of the ninflammatory reaction). In order to achieve normal growth and development there nmust be at least 120-150 kcal / kg per day.

5. Supply of nantioxidant protection. There is the immaturity of enzyme mechanisms in preterm ninfants. Animal studies and human biological material confirm the effectiveness nof superoxide dismutase and catalase, the result of which is manifested ndecreasing of cell damage, increasing survival, and possibly the prevention or nreduction in the severity of barotrauma. Today GCS are usedthe postnatal nperiod, not only for prevention of BPD, but for treatment of already formed ndisease.

 

                            Therapeutic nactivities:

1. System GCS nstabilize cellular and lysosomal membranes, increases surfactant synthesis, nincreases the concentration of vitamin A in serum, inhibit prostaglandins and nleukotrienes, reduce swelling of lung tissue and improve microcirculation iit. Currently, there is intensive studing of the role of inhaled GCS n(beclomethasone, budesonide, flyuticazon) as an alternative to systemic GCS, or nas a component of systemic steroid therapy. The available data are ncontradictory: some researchers prefer inhalation dexamethasone, others do not nconfirm the benefits of its application.

 

   

Flixotide

    

 

                    Steroid therapy involves ntwo options: early administration of steroids prevents the formation of BPD n(late first – early second week of life when on the background of persistent npulmonary edema appears interstitial emphysema) and  treats already established BPD (from the nsecond month of life). Routine use of dexamethasone in the treatment of BPD is nnot currently recommended because of the many negative side effects. Its nappointment is justified only when there is extreme severity of pulmonary nsymptoms.

2. Inhaled nβ₂-adrenomimetics also found their application in the treatment nof BPD. Salbutamol is a specific agonist of β₂-receptors and ncurrently enjoys high popularity in the treatment of BPD. Thanks nbronchodilatory effect it reduces bronchial resistance and increases the npermeability of the bronchi. However, since the first weeks of life expressed nrelaxation of smooth muscles of the bronchi is absent, early salbutamol ninhalation therapy is not considered justified.

 

3. Systemic nbronchodilators, which are the most commonly used in the treatment of children with nBPD, include methylxanthines – aminophylline, theophylline, caffeine (more nrarely).

 

  

4. Pulmonary nvasodilators: nifedipine (calcium channel blockers). A single oral dose of nnifedipine (0.5 mg / kg) reduces vascular resistance in the lungs and increases ncardiac output in older children with severe vascular hypertension due to BPD.

5. Antibiotic: nA number of studies in recent years distinguished Ureoplasma urealyticum as a nfactor contributing to the development of BPD. The results of clinical trials ndemonstrate reduction in the severity of the disease during therapy with nmacrolides.

 

 

                         BRONCHIAL ASTHMA

 

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

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

 

 

                                       Etiology and pathogenesis.

 

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

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

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

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

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

             The modern theory of the npathogenesis of asthma is the concept of allergic inflammation, which has nbecome an integrating, connecting the mediator (histamine), lipid membranes – nreceptor (β₂ – adrenergic receptors), neurovegetative n(vagotonia), reagine (Ig E) and other concepts. Development of suffocation is nconditioned directly by three major pathophysiological mechanisms: nbronchospasm, edema of bronchial mucosa and hypersecretion of bronchial glands. n

                            

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

              

                                                   n

                                                 nClassification of bronchial asthma

 

               The severity of asthma is nclassified on the basis of complex clinical and functional signs of bronchial nobstruction. The physician evaluates the frequency, severity and duration of nattacks of expiratory dyspnea, patient’s condition during the period betweeattacks, severity, variabillity, and repayment of functional bronchial nobstruction, response to treatment. Evaluation of functional indicators for ndetermining the severity of the disease is carried out in the absence of nepisodes expiratory dyspnea. According to this classification, the patient’s ncondition is determined by the degrees of seriousness of bronchial asthma. So nthere are  intermittent (episodic) ncourse; persistent (constant) course: mild, moderate and severe.

 

                The National Asthma Educatioand Prevention Program Expert Panel Report II (EPR-2), “Guidelines for the nDiagnosis and Management of Asthma,” highlight the importance of correctly ndiagnosing asthma. To establish the diagnosis of asthma, the clinician must establish nthe following: (a) episodic symptoms of airflow obstruction are present, (b) nairflow obstruction or symptoms are at least partially reversible, and (c) nalternative diagnoses are excluded.

                  The severity of asthma is nclassified as mild intermittent, mild persistent, moderate persistent, or nsevere persistent, according to the frequency and severity of symptoms, nincluding nocturnal symptoms, characteristics of acute episodes, and pulmonary nfunction.

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

                           Features of the categories include the following:

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

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

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

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

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

 

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

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

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

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

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

 

                                                           nClinic

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

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

 

                                        

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

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

                        Diagnostic criteria

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

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

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

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

                    –Physical examination ithe absence of an acute episode (eg, during an outpatient visit between acute nepisodes)

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

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

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

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

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

 

                            Barrel thorax

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

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

 

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

 

 

 

 

 

 

 

 

 

 

 

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

 

“Rabbit nose” of allergic rhinitis. (From Marks M: Physical nSigns of Allergy of the Respiratory Tract in Children. New York, AmericaCollege of Allergy, Asthma and Immunology, 1990.)

 

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

 

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

 

               

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

 

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

 

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

Wheezing: 

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

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

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

                In exercise-induced or nnocturnal asthma, wheezing may be present after exercise or during the night, nrespectively.

Coughing: Cough may be nthe only symptom of asthma, especially in cases of exercise-induced or nnocturnal asthma. Usually, the cough is nonproductive and nonparoxysmal. Also, ncoughing may be present with wheezing. Children with nocturnal asthma tend to ncough after midnight, during the early hours of morning.

Chest tightness: A nhistory of tightness or pain in the chest may be present with or without other nsymptoms of asthma, especially in exercise-induced or nocturnal asthma.

Other nonspecific symptoms: nInfants or young children may have history of recurrent bronchitis, nbronchiolitis, or pneumonia; a persistent cough with colds; and/or recurrent ncroup or chest rattling. Most children with chronic or recurrent bronchitis nhave asthma. Asthma is the most common underlying diagnosis in children with nrecurrent pneumonia. Older children may have a history of chest tightness and/or nrecurrent chest congestion.

                 During an acute episode, nsymptoms vary according to the severity.

Symptoms during a mild episode: nPatients may be breathless after physical activity such as walking. They catalk in sentences and lie down, and they may be agitated.

Symptoms during a moderate severe nepisode: Patients are breathless while talking. Infants have nfeeding difficulties and a softer, shorter cry.

Symptoms during a severe episode: nPatients are breathless during rest, are not interested in feeding, sit nupright, talk in words (not sentences), and are usually agitated.

Symptoms with imminent respiratory narrest (in addition to the aforementioned symptoms): The nchild is drowsy and confused. However, adolescents may not have these symptoms nuntil they are in frank respiratory failure.

Additional data. Despite the nfact that lung function tests are not decisive in the diagnosis, they help nassess the severity of airway obstruction and subsequent response to therapy ichronic and acute situations. VC, FVC,, FEV, nthe maximum air velocity in the middle of expiration, the maximum expiratory nflow rate (test Tiffno), FEV / VC decrease, residual volume (RV) and total lung ncapacity (TLC) increase  during episodes nof obstruction. Reduced FVC <25% of the proper or <0,75 after the nappointment of bronchodilator indicates the severity of the disease.

 Pulmonary nfunction test (PFT) results are not reliable in patients nyounger than 5 years. In young children (3-6 y) and older children who can’t nperform the conventional spirometry maneuver, newer techniques, such as nmeasurement of airway resistance using impulse oscillometry system, are being ntried. Measurement of airway resistance before and after a dose of inhaled nbronchodilator may help to diagnose bronchodilator responsive airway nobstruction.

Spirometry: nIn a typical case, an obstructive defect is present in the form of normal nforced vital capacity (FVC), reduced FEV1, and reduced forced expiratory flow nover 25-75% of the FVC (FEF 25-75). The flow-volume loop can be concave. nDocumentation of reversibility of airway obstruction after bronchodilator ntherapy is central to the definition of asthma. FEF 25-75 is a sensitive nindicator of obstruction and may be the only abnormality in a child with mild ndisease. In an outpatient or office setting, measurement of the peak flow rate nby using a peak flow meter can provide useful information about obstruction ithe large airways. Take care to ensure maximum patient effort. However, a nnormal peak flow rate does not necessarily mean a lack of airway obstruction.

   n   Spirograph

 

Plethysmography: Patients with chronic persistent nasthma may have hyperinflation, as evidenced by an increased total lung ncapacity (TLC) at plethysmography. Increased residual volume (RV) and nfunctional residual capacity (FRC) with normal TLC suggests air trapping. nAirway resistance is increased when significant obstruction is present.

 

 Air Displacement Plethysmography (ADP)

Bronchial provocation tests: Bronchial nprovocation tests may be performed to diagnose BHR. These tests are performed nin specialized laboratories by specially trained personnel to document airway nhyperresponsiveness to substances (eg, methacholine, histamine). Increasing ndoses of provocation agents are given, and FEV1 is measured. The endpoint is a n20% decrease in FEV1 (PD20).

Exercise challenge: In a patient with a history of nexercise-induced symptoms (eg, cough, wheeze, chest tightness or pain), the ndiagnosis of asthma can be confirmed with the exercise challenge. In a patient nof appropriate age (usually >6 y), the procedure involves baseline nspirometry followed by exercise on a treadmill or bicycle to a heart rate ngreater than 60% of the predicted maximum, with monitoring of the nelectrocardiogram and oxyhemoglobin saturation. The patient should be breathing ncold, dry air during the exercise to increase the yield of the study. nSpirographic findings and the PEF rate (PEFR) are determined immediately after nthe exercise period and at 3, 5, 10, 15, and 20 minutes after the first nmeasurement. The maximal decrease in lung function is calculated by using the nlowest postexercise and highest preexercise values. The reversibility of airway nobstruction can be assessed by administering aerosolized bronchodilators.

Blood testing: Eosinophil counts and IgE levels may nhelp when allergic factors are suspected.

Recent evidence suggests the nusefulness of measuring the fraction of nexhaled nitric oxide (FeNO) as a noninvasive marker of airway inflammation, nin order to adjust the dose of inhaled corticosteroids treatment. Currently nFeNO measurement, due to high cost of equipment, is used primarily as a nresearch tool.

Histologic Findings.

Asthma is an inflammatory ndisease characterized by the recruitment of inflammatory cells, vascular ncongestion, increased vascular permeability, increased tissue volume, and the npresence of an exudate. Eosinophilic infiltration, a universal finding, is nconsidered a major marker of the inflammatory activity of the disease. Histologic nevaluations of the airways in a typical patient reveal infiltration with ninflammatory cells, narrowing of airway lumina, bronchial and bronchiolar nepithelial denudation, and mucus plugs. Additionally, a patient with severe nasthma may have a markedly thickened basement membrane and airway remodeling ithe form of subepithelial fibrosis and smooth muscle hypertrophy or nhyperplasia.

            Peakflowmetria nallows, though tentatively, to control state of the respiratory system and nhelps to some extent monitor of the effectiveness of treatment.

             Peakflowmeter

Portable spirometer MicroLoop (Micro Medical nLtd., UK) with color sensor screen.                      

             

Imaging Studies

Chest radiography: nInclude chest radiography in the initial workup if the asthma does not respond nto therapy as expected. In addition to typical findings of hyperinflation and nincreased bronchial markings, a chest radiograph may reveal evidence of nparenchymal disease, atelectasis, pneumonia, congenital anomaly, or a foreigbody. In a patient with an acute asthmatic episode that responds poorly to ntherapy, a chest radiograph helps in the diagnosis of complications such as npneumothorax or pneumomediastinum. Chest x-ray is not always necessary. It cadocument the increase of pulmonary volume, infiltrates areas due to atelectasis nof distal obturated airway, this feature is important in suspecting of their ninfection.

 

 

Asthma. nA. The typical X-ray data 9-year-old child.

 The inflation and increased lung pattern. B. n7-year-old child with a more pronounced changes. C. Side projection showing nswelling with flattening of the diaphragm and increased anteroposterior ndiameter at the top.

(From Edwards D III: The child who nwheezes. <IT+>In:<IT-> von Waldenburg Hilton S, Edwards DIII (eds): nPractical Pediatric Radiology, 2nd ed. Philadelphia, WB Saunders, 1994, p 106.)

 

Paranasal sinus radiography or CT scanning: Consider nusing these to rule out sinusitis.

                                                                      

 

 

 

 

 

Optical ncoregent tomograph of new generation

 

 

                             Computor ntomography. Emphysema.

               

a                           b                                 c               Chronic Sinusitis

Image 1a, b and c n(Computed Tomography): There is mucosal thickening of the right maxillary sinus nwith no bony obstruction or soft tissue changes. Associated with this is nmucosal thickening of the right ostiomeatal complex. The left maxillary antrum nand ostiomeatal complex are unremarkable.

 

If you take a lot of many nsmall highly stetoscops, combine them into one matrix, connect the computer you nwill get a unique instrument Deep Beeze. The equipment can also explore the nfunction of the lungs, the process of filling the air, all filling, nsynchronicity, regularity. The device allows playback frame by frame, draws ngraphics. The procedure is very simple, noninvasive, performed within 12 nseconds. Supplier-Rosslyn Medical.

 

 

Other Tests

Allergy testing: Allergy testing can be used to nidentify allergic factors that may significantly contribute to the asthma. Once nidentified, environmental factors (eg, dust mites, cockroaches, molds, animal ndander) and outdoor factors (eg, pollen, grass, trees, molds) may be controlled nor avoided to reduce asthmatic symptoms. Allergens for skin testing are nselected on the basis of suspected or known allergens identified from a ndetailed environmental history. Antihistamines can suppress the skin test nresults and should be discontinued for an appropriate period (according to the nduration of action) before allergy testing. Topical or systemic corticosteroids ndo not affect the skin reaction.

                  In the period of remission allergic nskin tests are conducted, positive analysis of which gives the possibility to nexclude contact with the causative allergen, that is the key of the recovery.

                                Allergic nprick text. (Courtesy of MR Sly, M.D.)

 

The analysis of sputum: eosinophilia, Kurshman spiral n(cylinders of the bronchioles), crystals Charcot – Leiden; neutrophilia proves nthe existence of bronchial infection.

 

 

                                                                                                       

A–eosinophyles

B– Charcot – Leiden crystals

C– Kurshman spiral

                                                                          n

Arterial blood gases: typical symptoms of hypoxemia during nattacks and is usually expressed in hypocapnia and respiratory alkalosis, a nnormal or increased partial pressure pCO₂ showes a significant nfatigue of respiratory muscles and airway obstruction.

 

                      Differential diagnosis

“Any wheezing” – is nnot bronchial asthma. Differentiated with CNS diseases, chronic bronchitis and n(or) emphysema, obstruction URT caused by foreign body, tumor, edema of the nlarynx, carcinoid tumors (usually followed by a crowing, but not wheezing), nrepeated emphysema, eosinophilic pneumonia, dysfunction of the vocal folds, nsystemic vasculitis with lesions of the lungs.

Clinically the most important nis differential diagnosis with bronchiolitis and laryngotracheal stenosis ndue to similar clinical picture.

 

Differential diagnostics

 attack of nbronchial asthma that laryngotracheal stenosis

n

Criteria	Bronchial asthma	Laryngotracheal stenosis
Background of process	Period of precursors	ARVI (parainfluenza)
Cough	Dry, with transition in moist one	Dry, barking
Temperature	Normal	Subfebrile
Change of voice	Absent	Hoarse of voice
Shortness of breath	Expiration	Inciter
Forsed position	Characteristically	Non characteristically
Auscultation	The loosened breathing, the prolonged inspiration, dry whistling and moist wheezes	Strict breathing Dry  wheezes
Percussion	Box sound	Pulmonary sound
“Mute” lights	Characteristically	Not characteristically

 

                                  Treatment of the patients

 

Medical Care

The goals of asthma therapy nare to prevent chronic and troublesome symptoms, maintaiormal or near-normal npulmonary function, maintaiormal physical activity levels (including exercise), nprevent recurrent exacerbations of asthma, and minimize the need for emergency ndepartment visits or hospitalizations, provide optimal pharmacotherapy with nminimal or no adverse effects, and meet the family’s expectations for asthma ncare.

Medical care includes ntreatment of acute asthmatic episodes and control of chronic symptoms, nincluding nocturnal and exercise-induced asthmatic symptoms. Pharmacologic management includes the nuse of control agents such as inhaled corticosteroids, inhaled cromolyn or nnedocromil, long-acting bronchodilators, theophylline, leukotriene modifiers, nand recently introduced strategies such as the use of anti-IgE antibodies. nRelief medications include short-acting bronchodilators, systemic ncorticosteroids, and ipratropium. Nonpharmacologic management includes measures nto improve patient compliance and adherence. For all but the most severely naffected patients, the ultimate goal is to prevent symptoms, minimize morbidity nfrom acute episodes, and prevent functional and psychological morbidity to nprovide a healthy (or near healthy) lifestyle appropriate to the age of child.

 

A step-down approach based othe asthma severity classification system emphasizes the initiation of nhigh-level therapy to establish prompt control and then decreasing therapy n(National Asthma Education and Prevention Program Expert Panel Report II, n1997). Treatment should be reviewed every 1-6 months; a gradual stepwise nreduction in treatment may be possible. If control is not maintained despite nadequate medication and adherence and the exclusion of contributing nenvironmental factors, increased therapy should be considered. Long- and nshort-term therapy is based on the severity of asthma, as follows:

ü Mild nintermittent asthma 

ü Long-term ncontrol: Usually, no daily medication is needed.

ü Quick nrelief: Short-acting bronchodilators in the form of inhaled beta2-agonists nshould be used as needed for symptom control.

The use of short-acting ninhaled beta₂-agonists more than 2 times a week may indicate the nneed to initiate long-term control therapy.

Mild persistent asthma 

Long-term control: nAnti-inflammatory treatment in the form of low-dose inhaled corticosteroids or nnonsteroidal agents (eg, cromolyn, nedocromil) is preferred. Some evidence nsuggests that leukotriene antagonists may be useful as first-line therapy ichildren. Recently, the use of montelukast was approved for children aged 2 nyears and older.

Quick relief: Short-acting nbronchodilators in the form of inhaled beta2-agonists should be used as needed nfor symptom control. Use of short-acting inhaled beta2-agonists on a daily nbasis or increasing use indicates the need for additional long-term therapy.

Moderate persistent asthma

Long-term control: Daily nanti-inflammatory treatment in the form of inhaled corticosteroids (medium ndose) is preferred. Otherwise, low- or medium-dose inhaled corticosteroids ncombined with a long-acting bronchodilator or leukotriene antagonist can be nused, especially for the control of nocturnal or exercise-induced asthmatic nsymptoms.

Quick relief: Short-acting nbronchodilators in the form of inhaled beta2-agonists should be used as needed nfor symptom control. The use of short-acting inhaled beta2-agonists on a daily nbasis or increasing use indicates the need for additional long-term therapy.

Severe persistent asthma 

Long-term control 

Daily anti-inflammatory ntreatment in the form of inhaled corticosteroids (high dose) is preferred. nOther medications, such as a long-acting bronchodilator leukotriene antagonist nor theophylline, can be added.

Patients with nmoderate-to-severe asthma who react to perennial allergens despite inhaled ncorticosteroids may benefit from omalizumab treatment. Two 52-week pivotal nPhase III clinical trials were designed to study asthma exacerbation reductioin 1071 patients with asthma (aged 12-76 y). The coprimary endpoint of each nstudy was the number of asthma exacerbations per patient during the nstable-steroid phase and the steroid-reduction phase. Patients were randomized nto receive subcutaneous omalizumab or placebo every 2-4 weeks. Inhaled ncorticosteroid doses were kept stable over the initial 16 weeks of treatment n(stable-steroid phase) and tapered during a further 12-week treatment period n(steroid-reduction phase).

In both pivotal clinical ntrials, when used as an add-on therapy to inhaled corticosteroids, omalizumab nreduced mean asthma exacerbations (ie, asthma attacks) per patient by 33%-75% nduring the stable-steroid phase and 33%-50% during the steroid-reduction phase. nReduction in asthma exacerbations was confirmed by improvements in other nmeasurements of asthma control, including symptom scores (eg, nocturnal nawakenings, daytime asthma symptoms).

Quick relief: Short-acting nbronchodilators in the form of inhaled beta2-agonists should be used as needed nfor symptom control. The use of short-acting inhaled beta2-agonists on a daily nbasis or increasing use indicates the need for additional long-term therapy.

Acute severe asthmatic episode (status asthmaticus) 

Treatment goals are the nfollowing: 

Correction of significant nhypoxemia with supplemental oxygen: In severe cases, alveolar hypoventilatiorequires mechanically assisted ventilation.

Rapid reversal of airflow nobstruction by using repeated or continuous administration of an inhaled beta₂-agonist: nEarly administration of systemic corticosteroids (eg, oral prednisone or nintravenous methylprednisolone) is suggested in children with asthma that fails nto respond promptly and completely to inhaled beta2-agonists.

Reduction in the likelihood of nrecurrence of severe airflow obstruction by intensifying therapy: Often, a nshort course of systemic corticosteroids is helpful.

Achieving these goals requires nclose monitoring by means of serial clinical assessment and measurement of lung nfunction (in patients of appropriate ages) to quantify the severity of airflow nobstruction and its response to treatment. Improvement in FEV1 after 30 minutes nof treatment is significantly correlated with a broad range of indices of the nseverity of asthmatic exacerbations, and repeated measurement of airflow in the nemergency department can help reduce unnecessary admissions. Use of the peak nflow rate or FEV1 values, along with the patient’s history, current symptoms, nphysical findings, to guide treatment decisions is helpful in achieving the naforementioned goals. In using the PEF expressed as a percentage of the npatient’s best value, the effect of irreversible airflow obstruction should be nconsidered. For example, in a patient whose best peak flow rate is 160 L/min, a ndecrease of 40% represents severe and potentially life-threatening obstruction. n

 

                                      Consultations

Consider consultation with aallergist; ear, nose, and throat (ENT) specialist; or gastroenterologist. Aallergist may help with further evaluation and management when the history and nphysical examination findings suggest significant allergies (especially nsystemic involvement and allergies to dietary products). An ENT specialist may nhelp in managing chronic sinusitis. A gastroenterologist may help in excluding ngastroesophageal reflux.

 

                                     Diet

When a patient has major nallergies to dietary products, avoidance of particular foods may help. In the absence nof specific food allergies, dietary changes are not necessary. Unless ncompelling evidence for a specific allergy exists, milk products do not have to nbe avoided.

 

                                  Activity

One of the goals of therapy is nto adequately control exercise-induced asthmatic symptoms so that physical nactivity is not restricted.

 

                             Medication

Current treatment of asthma nincludes the use of relievers, such as beta-adrenergic agonists, systemic corticosteroids, nand ipratropium, and controllers, such as cromolyn, nedocromil, inhaled ncorticosteroids, long-acting beta-agonists, theophylline, and leukotriene nmodifiers.

 

Drug Category: Bronchodilator, beta₂-agonists

 

 These agents act as bronchodilators, used to ntreat bronchospasm in acute asthmatic episodes, and used to prevent nbronchospasm associated with exercise-induced asthma or nocturnal asthma. nSeveral studies have suggested that short-acting beta₂-agonists such nas albuterol may produce adverse outcomes (eg, decreased peak flow or increased nrisk of exacerbations) in patients homozygous for arginine (Arg/Arg) at the n16th amino acid position of beta-adrenergic receptor gene compared with npatients homozygous for glycine (Gly-Gly). Recently, similar findings are nreported for long-acting beta₂-agonists (eg, salmeterol).

Albuterol sulfate (Proventil, nVentolin)   This beta₂-agonist nis the most commonly used bronchodilator that is available in multiple forms n(eg, solution for nebulization, metered-dose inhaler (MDI), oral solution). nThis is most commonly used in rescue therapy for acute asthmatic symptoms. nAlbuterol is used as needed, and prolonged use may be associated with ntachyphylaxis due to beta2-receptor downregulation and receptor nhyposensitivity.

Pediatric:

Oral inhaler: 90 mcg per ninhalation, 2 inhalations q4-6h; more inhalations may be used in severe, acute nepisodes; more frequent dosing can be used to treat acute symptoms

 Nebulizer: 2.5 mg via nebulization of 0.5% nsolution in 2-3 mL of sodium chloride solution q4-6h

     

 

 

Pirbuterol acetate (Maxair)  Available as a breath-actuated or ordinary ninhaler. The ease of administration with the breath-actuated device makes it aattractive choice in the treatment of acute symptoms in younger children who notherwise cannot use an MDI. Strength is 200 mcg per inhalation.

Oral inhalation: 1-2 ninhalations q4-6h; not to exceed 12 inhalations q24h

Drug Category: Nonracemic form of the beta₂-agonist albuterol

This nonracemic form of nalbuterol was recently introduced. One advantage is better efficacy; hence, nlower doses have a therapeutic effect, and a significant reduction in the nadverse effects associated with racemic albuterol (eg, muscle tremors, ntachycardia, hyperglycemia, hypokalemia) is reported.

Levalbuterol (Xopenex) Nonracemic nform of albuterol, levalbuterol (R isomer) is effective in smaller doses and is nreported to have fewer adverse effects (eg, tachycardia, hyperglycemia, nhypokalemia). The dose may be doubled in acute severe episodes when even a nslight increase in the bronchodilator response may make a big difference in the nmanagement strategy (eg, in avoiding patient ventilation).

 0.63 mg by nebulizer q8h

    

 

Drug Category: Long-acting beta₂-agonist

 Long-acting bronchodilators are not used for nthe treatment of acute bronchospasm. They are used for the preventive treatment nof nocturnal asthma or exercise-induced asthmatic symptoms, for example. nCurrently, 2 long-acting beta2-agonists are available in the United States: nsalmeterol (Serevent) and formoterol (Foradil). Salmeterol is discussed below. nSalmeterol is available as a combination of salmeterol and fluticasone (Advair) nin the United States. Advair has an expiration date of 30 days once the protective nwrapper is removed.

Salmeterol (Serevent Diskus) nThis long-acting preparation of a beta2-agonist is used primarily to treat nnocturnal or exercise-induced symptoms. It has no anti-inflammatory action and nis not indicated in the treatment of acute bronchospastic episodes. It may be nused as an adjunct to inhaled corticosteroids to reduce the potential adverse neffects of the steroids.

<12 years: Not established

>12 years: 1 inhalation of ninhalation powder (50 mcg) q12h; data

                  in children are limited

  

 

 

 

 

Drug Category: Methylxanthines

These agents are used for nlong-term control and prevention of symptoms, especially nocturnal symptoms.

Theophylline (Theo-24, nTheolair, Theo-Dur, Slo-bid) is available in short- and long-acting formulations. nBecause of the need to monitor the drug levels (see Precautions below), this nagent is used infrequently.

Initial dose: 10 mg/kg PO nsustained-release tablets and capsules; not to exceed 300 mg/d

 First dose adjustment: 13 mg/kg PO; not to nexceed 450 mg/d

 Second dose adjustment: 16 mg/kg PO; not to nexceed 600 mg/d

 

Drug Category: Mast cell stabilizers

  These agents block early and late asthmatic nresponses, interfere with chloride channels, stabilize the mast cell membrane, nand inhibit the activation and release of mediators from eosinophils and nepithelial cells. They inhibit acute responses to cold air, exercise, and nsulfur dioxide.

Cromolyn sodium (Intal), nnedocromil sodium (Tilade). These nonsteroidal anti-inflammatory agents are nused primarily in preventive therapy.

Cromolyn: 20 mg in 2 mL nebulizer nsolution q6-8h

 Nedocromil: 2-4 inhalations bid/tid; n1.75 mg/actuation

 

  Intal   – cromolyn sodium

   Tilade   n– nedocromil

 

Drug Category: Corticosteroids

Steroids are the most potent anti-inflammatory nagents. Inhaled forms are topically active, poorly absorbed, and least likely nto cause adverse effects. No study has shown significant toxicity with inhaled nsteroid use in children at doses less than the equivalent of 400 mcg of beclomethasone nper day. They are used for long-term control of symptoms and for the nsuppression, control, and reversal of inflammation. Inhaled forms reduce the nneed for systemic corticosteroids. They block late asthmatic response to nallergens; reduce airway hyperresponsiveness; inhibit cytokine production, nadhesion protein activation, and inflammatory cell migration and activation; nand reverse beta2-receptor downregulation and subsensitivity (in acute nasthmatic episodes with long-term beta2-agonist use). 

 

Inhaled steroids include nbeclomethasone, triamcinolone, flunisolide, fluticasone, and budesonide.

Beclomethasone (Beclovent, nVanceril, QVAR)  Inhibits nbronchoconstriction mechanisms; causes direct smooth muscle relaxation; and may ndecrease the number and activity of inflammatory cells, which, in turn, ndecreases airway hyperresponsiveness.

Low dose: 84-336 mcg/d (42 nmcg/oral inhalation, 2-8 inhalations q24h)

 Medium dose: 336-672 mcg/d (42 mcg/oral ninhalations, 8-16

                     inhalations q24h)

 High dose: >672 mcg/d (42 mcg/oral ninhalation, >16 inhalations q24h)

 

                      

 

Fluticasone (Flovent) has nextremely potent vasoconstrictive and anti-inflammatory activity. Has a weak nhypothalamic-pituitary adrenocortical axis inhibitory potency when applied ntopically.

Low dose: 88-176 mcg/d (44 nmcg/oral inhalation, 2-4 inhalations q24h)

 Medium dose: 176-440 mcg/d (110 mcg/oral ninhalation, 2-4 inhalations

 q24h)

 High dose: >440 mcg/d (110 mcg/oral ninhalation, >4 inhalations q24h or 220

 mcg/oral inhalation, 2 inhalations q24h)

 

 

Budesonide (Pulmicort nTurbuhaler or Respules)  Has extremely npotent vasoconstrictive and anti-inflammatory activity. Has a weak nhypothalamic-pituitary adrenocortical axis inhibitory potency when applied ntopically. Pulmicort is available in a powder inhaler (200 mcg per oral ninhalation) or as a nebulized susp (ie, Respules).

MDI: Low dose: 100-200 mcg/d n(1 inhalation q24h)

 Medium dose: 200-400 mcg/d (1-2 ninhalation q24h)

 High dose: >400 mcg/d (>2 ninhalations q24h)

 Nebulizer (inhalation susp): 0.25-0.5 mg bid; nnot to exceed 1 mg/d

         

Drug Category: Systemic corticosteroids

 These agents are used for short courses (3-10 nd) to gain prompt control of inadequately controlled acute asthmatic episodes. nThey are also used for long-term prevention of symptoms in severe persistent nasthma as well as for suppression, control, and reversal of inflammation. nFrequent and repetitive use of beta2-agonists has been associated with nbeta2-receptor subsensitivity and downregulation; these processes are reversed nwith corticosteroids.

Higher-dose corticosteroids nhave no advantage in severe asthma exacerbations, and intravenous nadministration has no advantage over oral therapy, provided that ngastrointestinal transit time or absorption is not impaired. The usual regimeis to continue frequent multiple daily dosing until the FEV1 or PEF is 50% of nthe predicted or personal best values; then, the dose is changed to twice ndaily. This usually occurs within 48 hours.

Prednisone (Deltasone, nOrasone) and prednisolone (Pediapred, Prelone, Orapred) — Immunosuppressants nfor the treatment of autoimmune disorders; may decrease inflammation by nreversing increased capillary permeability and suppressing PMN activity.

1-2 mg/kg/d PO for 3-10 d; not nto exceed 60-80 mg/d

 

 

Methylprednisolone n(Solu-Medrol)  May decrease inflammatioby reversing increased capillary permeability and suppressing PMN activity.

1 mg/kg IV q6h

 

 

 

Drug Category: Leukotriene modifier

 Knowledge that leukotrienes cause nbronchospasm, increased vascular permeability, mucosal edema, and inflammatory ncell infiltration leads to the concept of modifying their action by using npharmacologic agents. These are either 5-lipoxygenase inhibitors or leukotriene-receptor nantagonists.

Zafirlukast (Accolate).  It is a selective competitive inhibitor of nLTD4, LTE4 receptors.

5-11 years: 10 mg PO bid

 >12 years: Administer as in adults

 

 

Montelukast (Singulair)   It is a last agent introduced in its class. nThe advantages are that it is chewable, it has a once-a-day dosing, and it has nno significant adverse effects.

12-23 months: 1 packet of 4 mg noral granules PO hs

 2-6 years: 4 mg PO hs

 6-14 years: 5 mg PO hs

 >14 years: Administer as in adults

 

Drug Category: Monoclonal antibody

  These agents bind selectively to human IgE othe surface of mast cells

and basophils.

Omalizumab (Xolair)  Recombinant, DNA-derived, humanized IgG nmonoclonal antibody that binds selectively to human IgE on surface of mast ncells and basophils. Reduces mediator release, which promotes allergic nresponse. Indicated for moderate-to-severe persistent asthma in patients who nreact to perennial allergens in whom symptoms are not controlled by inhaled ncorticosteroids.

<12 years: Not established

>12 years: 150-375 mg SC nq2-4wk; inject slowly over 5-10 s because of viscosity; not to exceed 150 mg nper injection site

 Precise dose and frequency established by nserum total IgE level (IU/mL)

                                  ASTHMATIC nSTATE

 

The asthmatic state is nthe attack of asthma, which lasts more than 6–10 hours and resistant to nsympatomimetics and methylxantins. It is characterized by total nbronchoobstruction on a background of refraction of b₂-adrenoreceptors with progress of hypoxia, nhypercapnia, decompensative acidosis, dehydration and development of acute ncardiac insufficiency of a right-heart type. In the process of development of nthe asthmatic state three stages are selected: relative indemnification, ndecompensation and hypoxemic comma.

 

Diagnostic ncriteria of asthmatic status

1. nProtracted attack of bronchial asthma, which nis not cured during 6 hears

    and nanymore.

2. nResistens to sympatomimetics.

3. Violatioof drainage function of bronchial tubes.

4. Development hypoxemia –  РаО₂  – 60 nml Hg, hypercarpnia – РаСО₂  60 ml Hg.

 

 

 

                                         Clinic.

 I stage of the asthmatic status n(relative compensation). Forced sitting  position, leaning against hands, tachypnoe with nthe considerably prolonged inspiration, attack cough with much amount of viscid nphlegm which is badly deleted. Skinis pale, cyanosys of lips, nasolips ntriangle, acro– nor general cyanosys. A thorax is emphysematous, the excursion  is limited, above lungs percussion box sound. nPlenty of the  distance wheezes icomparisone with little amount of  dry nwheezes, the loosened breathing in lungs. The border of heart is not determined, nare low, systolic murmur on an apex, tachycardia. A liver is enlarged, sickly. nArterial pressure is decreased.

 

                      Help on prehospital stage

1.             nDo not use of symdatomimetics!

2.             nTo provide access of fresh air.

3.             nTo release from squeezing clothes.

4.             nOxygentherapy:  moistened air through a mask.

5.             n2,4 % solution of Euphyllini in dose nof a 5 mg/kg of  mass of

                    intravenously streamly on a n15 –20 ml of isotonic  solution of sodium

                   chloride.

6.             n2 % solution of No-spani a 1 mg/кг nmass on dose intramuscular.

7.             n3 % solution of Prednisoloni 2-3 nmg/kg of the masses (Hydrocortisoni

                        10-15 mg/kg) nintramuscular or intravenously streamly.

8.             nUrgent hospitalization.

 

Help on a nhospital stage

1.             nDo not use sympatomimetics!

2.             nTo provide access of fresh air.

3.             nOxygentherapy optimum n40 % by the moistened oxygen constantly.

4.             n3 % solution of Prednisoloni in dose n2-3 mg/kg of  the mass

                      intravenously streamly oa 5-10 ml of  isotonic  solution of sodium

                     chloride.

5.             n2 % solution of No-spani  1 mg/kg of  nmass on dose intramuscular

                     or intravenously streamly nslowly.

6.             nSolution of Corgliconi 0,06 % or nStrophantini 0,05 % 0,1 ml per the year

                       of life, but not more nthan 0,3-0,4 ml on a 5-10 ml isotonic  nsolution of

                      sodium  chloride  nintravenously streamly.

7.             nCocarboxylazae 50-100 mg, 5 % nsolution of sodium ascorbinati 2,0-5,0

                    ml, Panangini 0,5 ml per nyear of life of intravenously streamly in

                   separate syringe .

8.             n2,4 % solution of Euphyllini 7-10 nmg/kg of  mass on a 200 ml of isotonic

                      solution of sodium  chloride intravenously with a next continuous

                      tranfusion on Euphyllinization by nintravenously infusion of 2,4 %

                      solution of Euphyllini at na speed of 0,7 mg/kg/hour on isotonic  nsolution

                     of sodium  chloride, but not more than 24 mg/kg/day for nthe children

                    upto 9 years and 20 nmg/kg/day for children  senior than  9 years.

9.             nHeparini 200-300 U/day on 4 nintravenous stream injection every 6 hours.

10.        nReopoliglucini 150-200 ml nintravenously in drops.

11.        nIn default of effect in 2 hours o nrepeate intravenous stream injection of

                     Prednisolone 2-3 mg/kg nof  the masses or Hydrocortisoni 10-15 nmg/kg

                    of  mass.

12.        nAlkaline drink: mineral water, 1 % nsolution of soda, milk with a soda.

                    Intravenous  injection of 4 % solution of sodium nbicarbonatis only under

                    the control of  acid – alkaline equilibrium indexes.

13.        nAbsence of effect after the repeated ninjection  of glucocorticoids testifies

                     to transition of the nasthmatic state in the ІІ stage.

 

Clinic of the nІІ stage of the asthmatic status (decompensations). Child iconsciousness, excited or apathetical. General cyanosis of skin and mucus, a nperson is puffy, the veins of neck are swelling. Breathing is encreased, noisy nwith the prolonged inspiration and acute downing in of interribs intervals, nsupraclavicular and epigastrial areas, jugular pit with a limited excursion of nthorax. Percussion: bandbox sound. Breathing is sharply loosened with single nunsounding dry wheezes, in the lower areas of lungs breathing is not listened, nsyndrome of “mute lungs”. Таhycardia, pulse of the weak filling, unrhythmical. The ntones of heart are not determined, tones are deaf. Arterial pressure is nreduced. A liver is enlarged, sickly.

Help on prehospital stage

1.             nTo provide access of fresh air.

2.             nOxygentherapy:  moistened air through a mask.

3.             n2,4 % solution of Euphyllini in dose nof a 5 mg/kg of  mass intravenously

                    streamly on a 15-20 ml nof  isotonic  solution of sodium  chloride.

4.             n3 % solution of Prednisoloni in dose nof a 3-5 mg/kg of  mass or

                   Hydrocortisoni 15-25 mg/kg nof  mass intramuscular or intravenously

                   streamly.

5.             nUrgent hospitalization.

 

Help on  hospital stage

1.             nTo provide access of fresh air.

2.             nOxygentherapy: noptimum 40 % of the moistened oxygen constantly

                     through a mask.

3.             n3 % solution of Prednisoloni in dose nof  3-5 mg/kg of  mass or

                   Hydrocortisoni  15-25 mg/kg of  mass of intravenously streamly with the

                   repeated introduction after 1,5-2 hours idefault of effect.

4.             n2 % solution of No-spani 1 mg/kg of nmass in dose intramuscular or

                    intravenously streamly nslowly.

5.             nSolution of Corgliconi 0,06 % or nStrophantini 0,05 % in dose 0,1 ml per

                     the year of life, but not nmore than 0,3-0,4 ml intravenously streamly on a

                     5-10 ml of  isotonic solution of sodium  chloride.

6.             nCocarboxylazae 50-100 mg, panangini n0,5 ml per year of life, 5 %

                    solution of  sodium  nascorbinati 2,0-5,0 ml intravenously streamly in

                    separate syringes.

7.             n2,4 % solution of Euphyllini 7-10 nmg/kg of mass on a 200 ml of isotonic

                    solution of sodium  chloride of intravenously in drops. If nEuphyllini was

                   already entered at treatment nof I stage of the asthmatic status, continue

                   Euphyllinization at a speed nof 0,7 mg/kg/hour on isotonic solution of

                   sodium chloride 50 ml/ hour.

8.             nHeparini 200-300 Units/kg/days, ndivided in 4 injections, every 6 hours

                      intravenously streamly.

9.             nIn default of effect after the nrepeated introduction of glucocorticoids

                    urgent intubation with nbronchoscopy sanation and after that- artificial

                    ventilation.

10.        nOn artificial ventilation Euphyllinization must be ncontinued, repeat

                    introductions of nPrednisoloni every 1,5-2 hours in  dose nof  6-10 mg/kg

                   of  nmass.

11.        nMucolitic drugs endotrachially with nthe following lavagge of bronchial

                     tubes with bronchoscopy.

12.        nIntravenously 4 % solution of sodium nbycarbonatis only under the

                      control of indexes acid – nalkaline equilibrium.

13.        nHaemosorbtion, plazmopheresis.

 

It is not recommended to enter:

1.Antihistaminic drugs – Suprastini,Tavegili, Claritini.

2.Sedative drugs – Seduxeni, Sodium noxytirati , Aminasini.

3.Drugs nwith ephedrini – Solutani, Broncholitini.

4.Unselective b_2- -adrenomimetics – Astmopent, Alupent, Izadrin.

5.Prolonged b_2- -adrenomimetics – Salmeterol, Seretid.

 

 

 

 

ATTACK OF BRONCHIAL ASTHMA IN nCHILDREN

OF EARLY AGE

As a result nof anatomo-physiologic features of breathing organs  in the children of early age  the pathophysiologic mechanisms of nbronchoobstruction and  edema of mucus nmembrane of bronchial tubes and hypersecretion of bronchial glands come forward non the first plan. It is the reasone of  nmore gradual beginning and slow  ndevelopment of disease, “moist” character of asthma, less efficiency of nsympatomimetics.

 

Clinic. Trouble, crabbiness of child at the moderate nphenomena of general intoxication and normal temperature of body. Cyanosis  of lips, nasolibs triangle, acrocyanosis. nDyspnoe, noisy, with the prolonged inspiration and   distance wheezes. Downing in of interribs nintervals, supraclavicular areas, jugular pit. Attacks of underproductive, nsometimes attack cough. A thorax is emphizematous, at percussion above lungs nbandbox sound, at auscultation breathing is hard, with the prolonged ninspiration and dissipated dry and different moist wheezes. Таchycardia. A liver is often enlarged. There can be neozinophylia in the general analysis of   nblood, sometimes there is moderate neutrophyl leucytosis. On the X-ray nexamination of thorax organs pulmonary  npicture is strengthening , areas of promoted pneumatisation without of ninfiltrative changes in lungs.

 

                            Further Inpatient Care

Admit patients for treatment of nacute severe episodes if they are unresponsive to outpatient care (eg, they nhave worsening bronchospasm, hypoxia, evidence of respiratory failure).

Once the patient is admitted, nfurther investigations (eg, PFTs, allergy testing, and investigations to rule nout other associated conditions and complications) can be performed.

 

                                Further Outpatient Care

Regular follow-up visits n(1-6-mo intervals) are essential to ensure control and appropriate therapeutic nadjustments.

Outpatient visits should ninclude the following:

Ø Interval nhistory of asthmatic complaints, including history of acute episodes

Ø (eg, nseverity, measures and treatment taken, response to therapy)

Ø History nof nocturnal symptoms

Ø History nof symptoms with exercise and exercise tolerance

Ø Review nof medications, including use of rescue medications

Ø Review nof home-monitoring data (eg, symptom diary, peak flow meter

Ø readings, ndaily treatments)

Ø Patient nevaluation should include the following:

Ø Assessment nfor signs of bronchospasm and complications

Ø Evaluatioof associated conditions (eg, allergic rhinitis)

Ø Pulmonary nfunction testing (in appropriate age group)

Ø Address nissues of treatment adherence and avoidance of environmental

Ø triggers nand irritants.

Long-term asthma care pathways nthat incorporate the aforementioned factors can serve as roadmaps for nambulatory asthma care and help streamline outpatient care by different nproviders.

In the author’s asthma clinic, na member of the asthma care team sits with each patient to review the writteasthma care plan and to write and discuss in detail a rescue plan for acute nepisode, which includes instructions about identifying signs of acute episode, nusing rescue medications, monitoring, and contacting the asthma care team. nThese items are reviewed at each visit.

 

Inpatient & Outpatient Medications

ü Bronchodilators n(short- and long-acting)

ü Controlling nmedications (nonsteroidal, steroidal, newer agents such

             as leukotriene nmodifiers)

ü Medications nfor the treatment of associated conditions (antiallergy

               nmedications, nasal steroids for allergic rhinitis)

ü Rescue nmedications for use in acute episodes (short burst of steroids)

 

                              Transfer

         Any patient with a high risk of asthma nshould be referred to a specialist. The following may suggest a high risk:

§  History nof sudden severe exacerbations

§  History nof prior intubation for asthma

§  Admissioto an ICU because of asthma

§  Two nor more hospitalizations for asthma in the past year

§  Three nor more emergency department visits for asthma in the past year

§  Hospitalizatioor an emergency department visit for asthma within the

§  past nmonth

§  Use nof 2 or more canisters of inhaled short-acting beta₂-agonists per nmonth

§  Current nuse of systemic corticosteroids or recent withdrawal from

       systemic corticosteroids

The choice between a pediatric npulmonologist and an allergist may depend on local availability and practices. nA patient with frequent ICU admissions, previous intubation, and a history of ncomplicating factors or comorbidity (eg, cystic fibrosis) should be referred to na pediatric pulmonologist. When allergies are thought to significantly ncontribute to the morbidity, an allergist may be helpful.

 

Prevention

The goal of long-term therapy nis to prevent acute exacerbations.

The patient should avoid nexposure to environmental allergens and irritants that are identified during nthe evaluation.

Complications

§  Pneumothorax, nstatus asthmaticus with respiratory failure

§  Fixed n(nonreversible) airway obstruction

§  Death n

 

Prognosis

Of infants who wheeze with nURTIs, 60% are asymptomatic by age 6 years; however, children who have asthma (recurrent nsymptoms continuing at age 6 y) have airway reactivity later in childhood.

Some findings suggest a poor nprognosis if asthma develops in children younger than 3 years, unless it occurs nsolely in association with viral infections.

Individuals who have asthma nduring childhood have significantly lower FEV1 and airway reactivity and more npersistent bronchospastic symptoms than those with infection-associated nwheezing.

Children with mild asthma who nare asymptomatic between attacks are likely to improve and be symptom-free nlater in life.

Children with asthma appear to nhave less severe symptoms as they enter adolescence, but half of these childrecontinue to have asthma.

Asthma has a tendency to remit nduring puberty, with a somewhat earlier remission in girls. However, compared nwith men, women have more BHR.

 

                    Patient Education

Patient and parent educatioshould include instructions on how to use medications and devices (eg, spacers, nnebulizers, MDIs). The patient’s MDI technique should be assessed on every nvisit.

Discuss the management plan, nwhich includes instructions about the use of medications, precautions with drug nand/or device usage, monitoring symptoms and their severity (peak flow meter nreading), and identifying potential adverse effects and necessary actions.

Write and discuss in detail a nrescue plan for an acute episode. This plan should include instructions for nidentifying signs of an acute attack, using rescue medications, monitoring, and ncontacting the asthma care team.

Parents should understand that nasthma is a chronic disorder with acute exacerbations; hence, continuity of nmanagement with active participation by the patient and/or parents and ninteraction with asthma care medical personnel is important.

Emphasize the importance of ncompliance with and adherence to treatment.

Incorporate the concept of nexpecting full control of symptoms, including nocturnal and exercise-induced nsymptoms, in the management plans and goals (for all but the most severely naffected patients).

Avoid unnecessary restrictions nin the lifestyle of the child or family. Expect the child to participate irecreational activities and sports and to attend school as usual.

 

                  ASPIRATION SYNDROME

 

One of the most common causes nof BOS in infants – a syndrome of habitual microaspiration of liquid food nassociated with dysphagia, often in combination with gastro-oesophageal reflux. nUp to 30% of all cases of recurrent cough in infants are associated with naspiration syndrome. Determination of the cause may be difficult. Anamnestic ndata helps in the diagnosis of aspiration. Usually in these children there are nthe history and neurological symptoms such as attack coughing that develops ithe child during feeding, the appearance of dry or moist rales in the lungs nafter a meal. The diagnosis is confirmed after examining a patient in the nhospital.

 

FOREIGN BODIES IN  LUNGS, TRACHEA nAND BRONCHIAL TUBES

 

It is the acute nobstruction of respiratory tracts as a result of aspiration of foreign bodies  of different nature(organic, inorganic, nmetallic)  in the respiratory tracts n(larynx, trachea, bronchial tubes).  nDepending on the location  foreigbodies are divided into balloting, valvular (valve) and obturacting. Mechanical nobstructions   and laryngospasm  have the main role I pathogenesis.

Clinic. Polymorphic, depends on the level of localizatioof foreign body, its size and nform, time of stay in respiratory tracts. At the hit of foreign body in a larynx on a complete health attack of nstrong cough arises up, dyspnea, asphyxia, hoarse of voice. The clinical sings nchange as a result of motion of body. A diagnosis is due to laryngoscopy. The foreign body of trachea predetermines an exhausting cough, ncharacteristic noise of slamming as a result of its blow on trachea, dyspnea nattack .In the case of invasive penetration of foreigh body pain in chest, nblood phlegma occur. If there is aspiration of foreign body in main bronchus, symptoms are the same, as nwell as at the hit in a trachea. When it penetrates deeper, in the distal nregions of respiratory tracts, a cough becomes weaker. Obturation atelectasis nin the proper lobe with compensating emphysema of neighbouring lobe develops at nthe complete corking of bronchus. The incomplete corking valve stenosis and obturatioemphysema occur. Collection of anamnesis is purposeful important iestablishment of diagnosis. Roentgencontrastive foreign bodies, or indirect signs of aspiration of nnonroentgencontrastive bodies (atelectasis, acute emphysema of segment, lobe or    lung), appear at roentgenologic research, nthe Holtskneht – Jacobson symptom is exposed: displacement of mediastenum at ndeep inhalation in a sick side and at deep exhalation – in healthy. Foreign body of trachea and bronchial tubes is diagnosed nalso by bronchoscopy.

 

Help oprehospital stage

1.                nTo try to ndelete the foreign body. To take a child for feet, to drop downward by a head n(for a short time) and inflict a few blows on the back. The children of the nfirst year of life are laid on abdomen and face on the forearm of doctor, here nby forel and middle fingers a head and neck are fixed. A forearm together with na child is lowered downward on 60 ^O. By the rib of palm of right nhand short blows are dealed between shoulder-blades. For  elders  nchildren  the Heymlih method is nused : on the epigastrial area of child, which lies on a side, a doctor nlays  the palm of the left hand, by the nfist of right hand deals 5-8 short blows under the corner of 45 ^O idirection of diaphragm, or child which suffered, is clasped from behind of back nby  hands so that the right palm ncompresses in a fist was at level between umbilicus and sternum, and left palm n– over it, four sharp blows are done in this position, sending them insite and nupwards, causing an artificial cough.

2.                nWith aattempt to delete the review of mouth cavity foreign body by hands or pincers, nat possibility with direct laryngoscopy.

3.                nImmediate nhospitalization to otolaryngology unit. During transporting there must be the npromoted position, to quiet a child, oxygen therapy.

4.                nAt nineffective of previous measures and impossibility of rapid hospitalization, nthere is the risk of death from an asphyxia. So conicotomia or tracheostomy is nexecuted. Method of conicotomia: head of patient is maximally  backwards, feel an interval between thyroid nthat cricoid cartilages and with scalpel or another cutting object cut a skin, nand then conical ligamentum   itransversal position. In the opening hole tracheostomic, intubation or another ntube, which is in hands, are placed in order to provide access of air in a ntrachea.

Method of tracheostomy: bolster under the shoulders (not under a neck!) nof patient. A head is maximally background. The little turn of head causes the ndisplacement of trachea and cut her over not on a middle line and the wound of nesophagus. Local anaesthesia. Vertical cut of skin from a cricoid cartilage by length of 4-5 cm. If a neck is short ntransversal cut is used by length of 5-6 cm at level of 2-3 rings of trachea. After ndissection skins and fascia execute the subsequent baring of trachea only by a ndull way. Move away the isthmus of thyroid downward and do overhead tracheostomy. Before nsection a trachea is sewed by silk which serves as a holder. Interval betweecartilages is cutting by scalpel   higher nthan a holder, canulla is entered in trachea.

Chronic foreign body producing nbronchiectasis in a 2-year-old boy. He had a history of choking o”something” while playing outdoors. A productive cough, recurrent npneumonia, and finger clubbing developed over the next 9 months. Chest film n(<IT+>A<IT->) shows right lower lobe infiltrate. Bronchogram n(<IT+>B<IT->) shows nonfilling of anterior basilar segment n(<IT+>arrow<IT->) of right lung. The resected segment n(<IT+>C<IT->) contained a bronchiectatic cavity n(<IT+>arrow<IT->) with an aspirated grasshead n(<IT+>D<IT->). Recovery was complete after operation and included nresolution of severe clubbing. (From Hilman BC (ed): Pediatric Respiratory nDisease. Philadelphia, WB Saunders, 1993, p 519.)

 

Help on  nhospital stage

1.                nIf nforeign body is in a larynx – laryngoscopy must be done to its delete.

2.                nAt finding of foreign body in a trachea or nbronchial tubes – quickly

                     tracheobronchoscopy with nanesthesia.

3.                nAntibiotics nof wide spectrum of action.

 

 

                            ANOTHER PATHOLOGY THAT CAUSES BOS

                

                A large group of diseases that noccur with the manifestations of BOS, are hereditary metabolic.

            Hereditary deficiency α₁-antitrypsi(α₁-protease inhibitor) is a relatively rare disorder, ninherited by autosomal recessive type. The earliest complaint is shortness of nbreath that occurs without cough and sputum, which, however, may join later. nPercussion, auscultation and radiological findings are typical of pulmonary nemphysema: swelling of the chest, bandbox sound over the lungs, weak breathing, nincreased pneumatization of pulmonary pattern. At α₁-antitrypsideficiency obstruction occurs due to loss of elasticity, and not as a result of nbronchospasm. The diagnosis of α₁-antitrypsin deficiency is nconfirmed by decrease of its content in the blood (normal 20-30 IU / ml), nphenotype, genetic examination of relatives of the patient.

              Clinical manifestations of BOS at ncongenital malformations of the heart and blood vessels have certain similarity nwith acute obstructive bronchitis. The main mechanism for the development of nBOS is a compression or occlusion of bronchial obstruction. The main idiagnosis is clinical and instrumental examination of the cardiovascular system nwith obligatory echocardiography.

             Recently, problem of relevant nspread of tuberculosis among children becomes actual, which may be masked as nobstructive bronchitis. In such case will be a long-term symptoms of nintoxication, a history of frequent respiratory infections.

At nX-ray of the chest thqre will be marked narrowing of the lumen of the bronchi, nareas of atelectasis, emphysema, the presence of fistula with separation of caseous nmass. For the correct diagnosis the utmost importance has tuberculidiagnostics, as well as identification of the causative agent in the washing nwaters.

             Often, BOS may be detected in diseases nof the central and peripheral nervous system. In children with birth trauma, nCNS impairment, hypertension-hydrocephalic syndrome, with severe malformations nof the brain may be disrupted coordination of swallowing and sucking, which may nresult in aspiration of food (mostly liquid) with the development of BOS. At nmyopathy (amyotrophy Verdniga-Hoffmann disease, Oppenheim’s) dysphagia nassociated with paresis of the swallowing muscles occurs with subsequent ndevelopment of aspiration bronchitis. Swallowing disorders in these diseases nare wavelike nature: the periods of improvement are replaced by increasing naspiration, mainly in the background of ARVI. Increased respiration and a ndirect effect of viral infection on the neuro-muscular system may contribute to nviolations of swallowing, dyskinesia of bronchial tree with the development of npronounced bronhoconstriction.

Thus, nthe differential diagnosis of bronchial obstruction syndrome in children is aextremely important issue. The tactics to the patient, differential treatment nmeasures, which in turn determines the outcome of the disease depends on the ntimely establishment of the causes of bronchial obstruction.

 

Referens:

A – Basic:

1.     nPediatrics. Textbook. / O. V. Tiazhka, T. V. nPochinok, A. N. Antoshkina et al. / edited by O. Tiazhka – Vinnytsia : nNova Knyha Publishers, 2011 – 584 pp. : il.ISBN 978-966-382-355-3

2.     nNelson Textbook nof Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & nStanton, 2011, 2608.  ISBN: n978-080-892-420-3.

3.     Illustrated nTextbook of Paediatrics, 4th Edition.  nPublished by  Lissauer & nClayden, 2012, 552 p. ISBN: 978-072-343-566-2.

4.     Denial Bernstein. Pediatrics for medical Students. – nSecond edition, 2012. – 650 p.

 

B – Additional:

1.http://intranet.tdmu.edu.ua/data/kafedra/internal/pediatria2/classes_stud/шпитальна%20педіатрія/6%20курс/English/Theme%2002%20Differential%20diagnosis%20of%20bronchial%20obstruction%20syndrome%20in%20children.htm

2. http://www.merckmanuals.com/professional/index.html

3. Lichtenstein, et al. Pediatric Pneumonia. Emergency medicine nclinics of north America.  2010.

4. Barson.  nClinical manifestations and diagnosis of community-aquired pneumonia ichildren. UpToDate.com., 2009.