Showing posts with label Pneumonia. Show all posts
Showing posts with label Pneumonia. Show all posts

Tuesday, April 2, 2013

Differential Diagnosis Of Bronchial Obstructive Syndrome In Children

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

          
        BOS - is a leading sign, which brings together a group of acute, recurrent and chronic lung disease, but it is not an independent nosological form and could not appear as a diagnosis. It should be noted that the BOS is not synonymous with bronchospasm, although in many cases, bronchospasm is important, and sometimes a leading role in the genesis of the disease. Usually BOS is diagnosed in children of the first four years of life, but can be diagnosed in older age.
            In the genesis of bronchial obstruction are different pathogenetic mechanisms, which can be divided into:
• functional or reversible (bronchospasm, inflammatory infiltration, edema,  mucociliary insufficiency, hypersecretion of viscous mucus)
• irreversible (congenital stenosis of the bronchi, their obliteration, etc.).
            Peculiar features of the children of the first three years of life have played the certain role in the development of bronchial obstruction:
Þ   narrowness of the bronchi and the entire respiratory system greatly increases
     aerodynamic resistance. Thus, swelling of the bronchial mucosa by only 1mm
     causes an increase in resistance to air flow in the trachea more than 50%.
Þ   softness of cartilage bronchial tract
Þ   lack of rigidity of the bone structure of the thorax, freely reacting indrawing of
     accommodating places to increase the resistance in the airways
Þ   particular position and the structure of the diaphragm.


             BOS in children may be substantially aggravated by structural features of bronchial wall, such as a large number of goblet cells that produce mucus, and
increased viscosity of bronchial secretions associated with high levels of cialic acid.
       Early childhood is characterized by the imperfection of immunological mechanisms: significantly reduced the formation of interferon in the upper respiratory tract, serum immunoglobulin A, secretory immunoglobulin A, and reduced functional activity of T-immunity system.

                Influence of premorbid factors of acute obstructive bronchitis:
- Toxicosis of pregnancy                                        - Dystrophy
- Obstructed labor                                                   - Hyperplasia of the thymus
- Hypoxia in childbirth                                           - Early artificial feeding
- Perinatal encephalopathy                                     - A variety of abnormalities of
- Prematurity                                                                     constitution
- Burdened allergic history                                    - The respiratory disease at the age
- Bronchial hyperreactivity                                                 of 6-12 months
- Rickets                                                                 - The presence of atopy
A major disadvantage is the pollution of the environment.
                  
                          

The scheme of the basic mechanisms of bronchial obstruction.


1. material into bronchi (foreign body, mucous etc.)
2. edema of bronchial mucous membranes (obstructive dronchitis)
3. retraction of bronchial muscles (bronchial asthma)
4. compression out of bronchus (mediastinum tumor, dilatation of pulmonary artery
    at congenital heart diseases)

                                       Etiology
                 BOS usually is infectious-allergic nature. Among the viruses that most commonly cause BOS are respiratory syncytial virus (50%), then parainfluenza, rarely - influenza and adenovirus. Recently, in the development of BOS big role is due to intracellular pathogens. According to modern data, chlamydia and mycoplasma infection are determined in 20% of children with BOS. According to different authors, about 20-25% of bronchitis in children occur as an acute obstructive bronchitis (AOB), which is significantly higher than in adults.
               Especially high frequency of AOB is as a manifestation of acute respiratory infections (ARI) in infants. This is due to the fact that in the first half year of life 80% of the entire surface of the lungs is small bronchi (diameter less than 2mm), whereas a child 6 years old - already 20%. According to the Poiseul rule resistance of airways is inversely proportional to their radius in the 4-th degree. Obstructive syndrome of is the more probable in the distal lesion of the bronchi.

                                     

Pathogenesis
                      
                Regulation of bronchial tone is controlled by several physiological mechanisms, which include complex interactions receptor-cell component and mediators system. These include cholinergic, adrenergic, neurohumoral regulatory system and, of course, the development of inflammation. Interleukin-1 is the main mediator, initiating the acute phase of inflammation. It activates a cascade of immune reactions that contribute to the exit in the peripheral blood of type 1 mediators (histamine, serotonin and others).
               Histamine is released during an allergic reaction in the interaction of allergen with allergen IgE. In addition to histamine, a type 2 (eicosanoids) play an important role in the pathogenesis of inflammatory mediators. Under the action of cyclooxygenase from arachidonic acid there are synthesing prostaglandins, thromboxane and prostacyclin, while under the influence lipooxidaze - leukotrienes.
              The result is increased vascular permeability, leading to swelling of the mucous membrane of the bronchi, hypersecretion of viscous mucus, the development of bronchospasm. The main mechanism in the pathogenesis of bronchospasm is activation of cholinergic nerve fibers, leading to increased production of acetylcholine and increasing concentrations of gualinatecyclase, which promotes the flow of calcium ions into smooth muscle cells, thereby stimulating of bronhoconstriction. Stimulation of α2-adrenoceptor catecholamines, as well as an increased concentration of cAMP decreases the manifestations of bronchospasm.

                                    Clinics of BOS

             The clinical picture of BOS in children is primarily determined by factors of bronhoconstriction. As noted above, in most cases BOS is associated with manifestations of acute respiratory viral infection (acute obstructive bronchitis).  So body temperature is rised up early, catarrhal changes in the upper respiratory tract and violation of general condition of the child appear. The severity and the nature largely vary depending on what the agent has led to the disease. Signs expiratory breathing difficulties may occur as the first day of illness, and in the process of viral infection (3-5-day sickness). Gradually there is increasing the breathing frequency and duration of exhalation. Breathing becomes noisy and whistling, which is due to the fact that with the development of hypersecretion, the accumulation of secretions in the lumen of the bronchi due to shortness of breath and fever change viscosity of the secret - he "dries up", which leads to buzzing (low) and whistling (high) wheezes.
           The defeat of the bronchi is widespread, and therefore hard breathing with dry whistling and buzzing wheezing are equally audible over the entire surface of the thorax. Rales may be heard at a distance. The younger the child, the more frequently he has, in addition to dry, the moist medium bubbling rales. If in the genesis of bronchial obstruction a major role plays spastic component, it auscultative data over lungs is generally more diverse and labile during the day. With increasing dyspnea important role of supporting muscles becomes increasingly - retraction of the intercostal spaces, epigastric and supraclavicular fossa, bloating (voltage) of the nostrils. Often there are revealed perioral cyanosis, pallor of the skin, the child becomes restless, trying to adopt a sitting position, drawing on his hands.
              Respiratory failure more evident than the younger the child, but usually it is not more than II degree. On physical examination, in addition to scattered wheezes and hard breathing, there are the signs of lung swelling: narrowing boundaries of relative cardiac dullness, boxed shade percussion tone. The inflation of the lungs is a result of consequence wears small bronchial branches during expiration, which leads to the so-called ventilation emphysema. The volume of the lungs increases. The rib cage is constantly in a state of inspiration, which increases the anteroposterior size.
            Changes in peripheral blood correspond to the nature of viral infection. Bacterial flora is rarely overlapped - not more than 5%.
            Radiologically, in addition to strengthening bilateral lung pattern and expansion of the roots of the lungs there are revealed: lowness flattened dome of the diaphragm, increasing the transparency of lung fields, lengthening the lung fields, a horizontal arrangement of ribs on the radiograph, which mean the signs of swelling of the lungs.

                             Diseases accompanied by BOS

              There are the following groups of diseases accompanied by BOS:
• Diseases of the respiratory system – Infectious-inflammatory diseases (acute constrictive laryngotracheitis, bronchitis, bronchiolitis, pneumonia), allergic diseases (obstructive bronchitis, bronchial asthma), bronchopulmonary dysplasia, malformation of bronchopulmonary system, tumors of the trachea and bronchi.
• Foreign bodies of trachea, bronchus, esophagus.
• Diseases of the aspiration genesis (aspiration or obstructive bronchitis) – gastroesophageal reflux, tracheoesophageal fistula, malformations of the gastrointestinal tract and diaphragmatic hernia.
• Diseases of the cardiovascular system – Congenital and acquired (congenital heart disease with hypertension, pulmonary circulation, vascular anomalies, congenital Non-rheumatic carditis, etc.).
• Diseases of the central and peripheral nervous system (birth injury, myopathy, etc.).
• Hereditary anomalies of metabolism (cystic fibrosis, α1-antitrypsin deficiency, mucopolysaccharidosis).
• Congenital and acquired immunodeficiency states.
• Rare hereditary diseases.
• Other states – Injuries and burns, poisoning, the effects of various physical and chemical environmental factors, pressure on the trachea and bronchi of extrapulmonary origin (tumor, venereal disease).

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

BRONCOOBSTRUCTIVE SYNDROME IN PNEUMONIA


The edema of mucus membrane of bronchial tubes lies in the basis of syndrome, hyperproductions of phlegm and, in a less measure, bronchospasm, more frequent on a background of congenital or acquired hyperreactivity of bronchial tubes are also important factor. This syndrome is identified at acute bronchopneumonia and is the reason of respiratory insufficiency on a bronchoobstructive type, which quite often determines severity of the state and needs adequate oxygent therapy.
Clinic. Increase of temperature of body, trouble or oppression, crabbiness, pallor of skin with perioral and acrocyanosis, unproductive cough, controlled from distance wheezes, oral crepitation, shortness of breath, with prolonged one and hard exhalation, drowning in chest of intervals between ribs, another areas of chest.
Percussion reveals the tympanic sound with areas of short sound.
Auscultation: hard breathing with the prolonged exhalation, dissipated dry and moist wheezes, the locally loosened breathing with the isolated proof moist wheezes.

 

Help on prehospital stage
1.             To provide access of fresh air.
2.             To release from squeezing clothes.
3.             Clean oral cavity and larynx from mucus and  phlegma

                                                                        
              



 Apparatus for cleaning of nose

4.    Oxygentherapy with clean moistened oxygen through a mask or oxygen pillow.
5.    Inhalation of dosed aerosol of Atroventi (ipratromium-bromide) 1-2 through spenser.
6. Inhalation of dosed aerosol b2-antagonists of quick actions (Salbutamoli, Ventolini, Berotec) 1-2 doses through spenser 20 minutes during hour. When it is impossible to make inhalations- syrup, tablets of Salbutamoli or Terbutalini (Bricaniliу)  to children upto 1 year - 1 mg 3 times, 3-6 years – 2 mg 3 times, 7-15 years – 2-3 mg 3 times; Clentuberoli (Spiropent) – 0,005-0,02  3 times; Broncholitini to  children upto 3 years– half tea-spoon, 3-10 years  1 tea-spoon, elder 10 years is a 1 dessert-spoon 3 times per days.
7. Euphyllini 3-5 mg/kg  - 2,4 % solution of Euphyllini in that  dose  intravenously streamly on 10 ml of 10 %  glucose solution .
8. 3 % solution of Prednisoloni 1-2 mg/kg  intramuscular.
9. Hospitalization.

Help on a hospital stage
1. To provide access of fresh air.
2. To release from squeezing clothes.
3. Sucking with electrosucker mucus and phlegma from upper respiratory tracts.
4. Oxygenation therapy through a nasal catheter is the clean moistened oxygen during 20 minutes every 2 hours or 40 % oxygen constantly.

 
        Oxygenation therapy through a nasal catheter
 5. Inhalation of dosed to the aerosol of Atroventi (ipratromium-bromide) 1-2 dose through spenser.
6. Inhalation of dosed  aerosol b2-antagonists of quick actions (Salbutamoli (Ventolini, Berotec) 1-2 doses through spenser 20 minutes during hour. When it is impossible to make inhalations- syrup, tablets of Salbutamoli or Terbutalini (Bricaniliу) children upto 1 year - 1 mg 3 times, 3-6 years – 2 mg 3 times, 7-15 years – 2-3 mg 3 times; Clentuberoli (Spiropent) – 0,005-0,02   3 times; Broncholitini to  children upto 3 years– half tea-spoon, 3-10 years- 1 tea-spoon, elder 10 years is a 1 dessert-spoon 3 times per days.
                                 
                                
 7.  3 % solution of Prednisoloni 1-2 mg/kg of  masses  intravenously  streamly.
 8. 2,4 % solution of Euphyllini 0,15 ml/kg of mass of  intravenously  in drops on
       10 % glucose solution  10–15 ml/kg.
 9. Cocarboxilazae of a 5–10 mg/kg of mass on 5,0 ml of 10 % Glucose solution
      intravenously  streamly.
 10. 5 % solution of sodium ascorbinati 2 ml/kg of masses of   intravenously  streamly
        on 5,0 ml of  10 % glucose solution .
 11. Panangini 0,1 ml/kgh of masses on 5,0 ml of 10 % Glucose solution
       intravenously  streamly.
 12.  In default of effect  drops intravenously introduction of Prednisoloni 2 – 3 mg/kg of  the masses (Hydrocortisoni 10 – 15 mg/kg) on 10 % Glucose solution  a 10 – 15 ml/kg of  mass.
 13. Mucolytic drugs: salt–alkaline inhalations; Lasolvani,Acetylcycteini  in inhalations, syrup, tablets; Bromhexini  in syrup, tablets; Mucaltini in tablets.


        



Mucolytic inhalations



14. Vibromassage of thorax in drainage position with next active aspiration of
       phlegm.
15. Alkaline drink: solution 1 % sodium bycarbonati per day to drink 10 – 12 ml/kg of mass slightly.
                   

Emergency Therapy For Acute Respiratory Failure

Respiratory Failure (RF)
   Is  the pathological  state, at which breathing organs are unable to provide adequate saturation of organism by oxygen and destroy  carbon dioxide.

 Anatomic and physiological   features of respiratory organs
1.  High metabolism, greater necessities in oxygen, however less compensating possibilities of organs of breathing;
2. Uncomplete differentiation of tissues;
3. Narrow respiratory tracts;
4. Undevelopment of additional cavities of nose, absence of lower nasal passage;
5. Propensity to the edema of mucous - through large amount of   vessels (ventilation failure);
6. The features of larynx structure (tender of cartilaginous ring, narrow upper space, expressed submucous tissue) ® croup.

•Tender trachea, bronchial tubes, little amount of   elastic tissues ® narrowing of respiratory road ® swollen mucus, hypersecretion of bronchial glands ® obstructions (hypoventilation -emphysema);
Undevelopment of cilia epithelium ® propensity to violation of evacuation function of respiratory tract;
•Lungs sanguineous, small elastic and many connective tissue  ® restrictive RF (exudation, аtelectasis, emphysema);
•Horizontal placing of ribs, low retractive ability of diaphragm ® diminish of   the excursion of lungs.

                                    Etiology of RF
                      The reasons leading to the development of acute respiratory failure are a lot. The most frequent causes of respiratory failure are listed below.
                                     1. Obstructive type
a) Obstruction of the upper respiratory tract may occur when there are abnormalities of development (atresia choanae, Pierre Robin syndrome, stenosis of the larynx above the vocal cords), aspiration of gastric contents, or foreign body, infections (epiglottitis), allergic laryngism, the tissue changes (tumor, cyst, hypertrophy of tonsils).
b) Obstruction of the lower airways may occur when there are abnormalities of development (bronhomalacia, lobar Emphysema), aspiration (in the presence of traheoezophageal fistula, infections (mumps, bronchiolitis, pneumonia), inflammation, bronchospasm (asthma, bronchopulmonary dysplasia), as well as foreign bodies.
                        2. Restrictive violations

a) With the defeat of the parenchyma of the lungs. Hypoplasia of lung, RDS, pneumothorax, hemorrhage, pulmonary edema and pleurisy.
b) With the defeat of the chest wall. Diaphragmatic hernia, absence of ribs, hypoplasia and aplasia of the sternum, chest deformity (rickets), abdominal distension, kyphoscoliosis, trauma restricted mobility of the chest, severe myasthenia pseudoparalitic, muscular dystrophy, and obesity.
                                
                                 3. Diseases that lead to inadequate gas alveoli and
                                                        capillaries exchanges
                                       

a) Diseases of the violations of diffusion. Diffuse type of RF: lung edema, interstitial fibrosis, collagenosis, pneumonia (Pneumocystis carinii), desquamative interstitial pneumonia.
b) Diseases due to inhibition of the respiratory center (Ventilation type of RF). Traumatic brain injury, CNS infection, overdose of sedatives; severe asphyxia and tetanus.
                             
                      4. Other situations that contribute to the development of the
                          acute respiratory distress
a) An increase in hydrostatic pressure.
b) Congestive heart failure.
c) The excess of fluid injected.
d) Intestinal obstruction.
e) Chronic broncho-pulmonary diseases




Etiologic classification of respiratory insufficiency

1. RF related to the obstruction of respiratory tracts (larynx-, bronchiolo-, bronchospasm, foreing body);
2. RF as a result of violation of diffusion of gases through an alveolar-capillary membrane (pneumonias, chronic diseases of lungs);
3. RF related to the damage of respiratory system (trauma of thorax, pneumo- thorax);
4. RF of central genesis - arises up at the damage of cerebrum (edema of brain, meningitis, cranial-cerebral trauma);
5. RF conditioned by violation of neuro-muscular conductivity (poliomyelitis, myasthenia)

                                   Clinic of respiratory insufficiency


        
1. Disturbances of function of the external breathing: shortness of breath, difficulty of breathing, prolonged exhalation, participation of auxiliary muscles, nod motions by a head, blowing of nostrils, violation of rhythm of breathing (bradypnoe, pathological type of breathing);
      2. Signs of hypercapnia, hypoxia: tachycardia, decreased arterial pressure, pallor of skin, acrocyanosis, cyanosys, excitation or oppression of child;
     3. Signs of tissue hypoxia: pallor -gray color of skin, bradycardia, decreased arterial pressure and comma.
                      Clinical manifestations are divided into 3 groups.
                       1. Pulmonary symptoms
a) In infants and children with acute respiratory failure - tachypnea, violations of the depth and rhythm of respiratory movements, retraction of the intercostal spaces, the expansion of nostrils, cyanosis, sweating.
b) possible shortness of breath and wheezing.
                      2. Neurological symptoms.
As a result of increased sensitivity of the brain to hypoxemia there is developing headache, anxiety, irritability, convulsions, and sometimes coma.
                     3. Symptoms of the cardiovascular system.
 There are bradycardia and hypotension. Severe and /or prolonged
 respiratory failure can lead to heart  failure and pulmonary edema.
Clinical classification of respiratory insufficiency

  I   stage: the shortness of breath in rest is absent, perioral cyanosys, which increases at loading, PS: BR – 3,5-2,5: 1; РаО2 – 80-65 mm Hg
The ІІ stage: is   the shortness of breath in rests, perioral cyanosys, acrocyanosis permanent, participation of auxiliary musculature in the act of breathing, PS: BR – 2-1,5: 1
 РаО2 – 64-51mmHg
The ІІІ stage: is the expressed shortness of breath in rest, the unrhythmical breathing (paradoxical breathing), generalized cyanosys is permanent, does not disappear at breathing by oxygen;
 РаО2 – 50 and ¯


                   Respiratory failure in acute pneumonia is 3 degrees.
      At I degree respiratory insufficiency is compensated by hyperventilation, there are no breathing disorders. At II degree there are the clinical and laboratory signs of disorders of external respiration, hemodynamics, but they are subcompensated. At III degree decompensation is diagnosed, both external and internal respiration.

Spirography determines the speed and volume of breath



Clinical features of RDS in newborn

1.Tachypnoe (BR > 60),  bradypnoe (BR <35);
2. Cyanosys;
3. Retractions (drawing in of pliable places of chest);
4. Blowing of wings of nose;
5. Grants (expiration moan);
6. Disturbance of rhythm or breathing;
7. Reduced activity.

                               
                           Treatment of respiratory failure

           The treatment depends on the leading pathological process, as well as the degree of hypoxemia, pCO2 and pH. For the recovery there is necessary to liquidate respiratory failure (removal of foreign body, the causes of the collapse of the lung: pneumothorax, lobar emphysema, diaphragmatic hernia).

             1. Oxygenation should begin only after the removal of the contents of the airways and should be performed using mixtures containing a minimum amount of oxygen that allows to maintain an adequate level of arterial pO2 (> 60 mmHg). The use of excessive concentrations of O2, may provoke pulmonary edema, atelectasis, or lead to retinopathy in preterm infants. If resistant to treatment forms of hypoxemia are present it needs intubation for ensuring long-term positive pressure in the lungs.
               2. Liquidation of  the disorders in the lungs involves the removal of bronchial secretion, the appointment of bronchodilators, intubation, or connecting to a respiration apparatus.
                      a) Endotracheal or nasotraheal intubation is enough to eliminate
                       obstruction of the upper respiratory tract.
                       The correct location of the tube should be monitored auscultation
                       or X-ray.
                      b) Increasing the humidity of air reduces the viscosity of bronchial
                       secretion.
               3. Intubation and ventilation with positive pressure is needed in patients
                          with elevated values of pCO2, accompanied by respiratory acidosis.


   


                           
Referens:
A - Basic:
1.      Pediatrics. Textbook. / O. V. Tiazhka, T. V. Pochinok, A. N. Antoshkina et al. / edited by O. TiazhkaVinnytsia : Nova Knyha Publishers, 2011 – 584 pp. : il.
2.      ISBN 978-966-382-355-3Nelson Textbook of Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & Stanton, 2011, 2608.  ISBN: 978-080-892-420-3.
3.      Illustrated Textbook of Paediatrics, 4th Edition.  Published by  Lissauer & Clayden, 2012, 552 p. ISBN: 978-072-343-566-2.
4.      Denial Bernstein. Pediatrics for medical Students. – Second edition, 2012. – 650 p.
B - Additional: 1.http://intranet.tdmu.edu.ua/data/kafedra/internal/pediatria2/classes_stud/шпитальна%20педіатрія/6%20курс/English/Theme%2001%20Differential%20diagnosis%20of%20pneumonia%20in%20children.htm
2. http://www.merckmanuals.com/professional/index.html
3. Lichtenstein, et al. Pediatric Pneumonia. Emergency medicine clinics of north America.  2010.
4. Barson.  Clinical manifestations and diagnosis of community-aquired pneumonia in children. UpToDate.com., 2009.