Differential diagnosis of pneumonia in

June 26, 2024
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Differential diagnosis of pneumonia in

children. Complications of pneumonia.

Emergency aid in acute respiratory

failure in children.

 

                          

 

                      ACUTE PNEUMONIA

 

                 Pneumoniais an infectious inflammation in the lung tissue, which leads to disruption of gas exchange in the body of the child and the appearance of  respiratory failure.

 

             Actuality of acute pneumonia in infants and its high rate is due to:

1. A significant spread of the pathology in children of the first year of life ( 2%,  among children of the first three years – 0.5-0,6%).

2. Severity, chronization  of the  bronchopulmonary diseases.

3. High mortality rate, which is due to the fact that pneumonia is the primary cause of infant mortality (in the world nearly 5 million children die under the age of 5yrs per  year,  every 7 seconds one child dies from pneumonia).

 

                 Physicians of different professions  must know clinics, diagnosis, treatment of acute pneumonia in young children and be able to prevent this disease.

 

 

 

               The etiology, pathogenesis and morbid anatomy.

                     The anatomic and physiological features of the respiratory system in children are important factors that determine susceptibility to the emergence of pneumonia, induce its high frequency and the possibility of transition into the chronic form. The lower the age of the child, the more pronounced these features, the higher the risk of pneumonia, the severer it will be over.

            The anatomic and physiologic features that are important for the clinician are:

1) incompleteness of differentiation of tissues of respiratory system (lung inflammation occurs quickly and with more severe damage)

2) the relatively smaller size and narrow respiratory tract, the absence of the inferior concha until 4 yrs old, hypoplasia of the sphenoidal sinuses (reduction of gas exchange),

3) vulnerability, softness, rich vascularization of the mucosa, the tendency to edema (rapid violation of ventilation),

4) the rigidity of the cartilage ring, narrow subglottic larynx space (inflammation → respiratory failure → stenosis → croup);

5) softness, suppleness of the trachea and bronchi, a small number of elastic fibers (compression of the thymus, enlarged lymph nodes, forked aortic arch → stridor) cause that forced expiration results iarrowing of the space, and even collapse of the trachea and bronchi (mucous edema, hypersecretion of bronchial glands leads to obstruction of varying degrees of severity: a) obstructive hypoventilation b) emphysema c) atelectasis);

6) the propensity to rapid violation of the evacuation function of tracheobronchial ways (fragility, immaturity of ciliated epithelium, mild passive component of hypo- or hypertention types of dyskinesia);

7) a significant proportion of interstitial tissue in the lungs, little amount of elastic fibres, a lot of blood vessels, lung is less  air (expressed exudative inflammatory component, easy developing of atelectasis, emphysema);

8) the thorax is as in a constant inspiration phase in a horizontal arrangement of ribs, a small excursion of the lungs  (breathing is abdominal iature, so conditions such as meteorism, liver enlargement, the presence of air in the stomach, diaphragm muscle hypotonia drastically impede gas exchange and increase the severity of pneumonia).

       It must be emphasized that these anatomical and physiological features are the more pronounced in the small child’s age. That is why pneumonia develops more often in this period of life.

 

In the occurrence of the disease leading role, along with anatomical and physiological features, have the adverse external conditions (cooling, improper feeding, in particular, the artificial defects and health care, long stay in a damp location, etc.) and internal ( previous acute infectious diseases, rickets, malnutrition, anemia, exudative-catarrhal constitutional anomaly, birth trauma, asphyxia, etc.) environments. The state of reactivity of the body of the child and the defensive forces is important in the genesis and development of pneumonia.

 

ETIOLOGY

 

Community-acquired pneumonia are caused by:

– Children from 1 to 6 months.: Viruses (RS, parainfluenza)

    E. coli and other gram-negative pathogens, Staphylococci.

– Children from 6 months to 6 years: Pneumococcus, H.influenzae type B.

– Children from 7 to 15 years: Streptococci, Pneumococci.

 

Nosocomial:

Escherichia coli, K.pneumoniae, Proteus, Enterobacteria, Pseudomonas, Staphylococcus.

 

Acute destructive pneumonia (ADP):

Staphylococcus, Pneumococcus, viral-microbial associations, Proteus, Legionella, Pseudomonas aeruginosa, Klebsiella, Haemophilus influenzae.

 

Factors that precede the appearance of pneumonia and contribute to its development:

Ø Morphological and functional immaturity of the early age childs and

                   unfavorable premorbid state (birth defects of respiratory and enzyme

                    systems, the anomalies of the constitution, prematurity, hypo – and

                   paratrophy, rickets)

Ø Supercooling of the organism

Ø For acute pneumonia: inappropriate antibiotic therapy, respiratory dysbacteriosis,   bad premorbid state, the aggressive agent and its significant

 

PATHOGENESIS

                  Unfavourable external and internal environments contribute to disruption of barrier function of mucous membrane of the bronchi, reduce local immunity of lung tissue and cause deterioration of the evacuation function of the bronchial tree. The pathogen agent penetrates bronchogenically (aerogenically), hematogenically or rarely lymphogenically, causing changes in the mucous membrane of the respiratory tract. Pathogens may be bacteria (pneumococci, streptococci, staphylococci, Gram-negative flora), viruses, fungi, parasites (pneumocysts), an association of various pathogens.

                 Factors, preceding and contributing to disease, create favorable conditions for life and reproduction of pathogen that causes inflammation. In the pathological process mucosa of the bronchi and bronchioles, intermediate and alveolar tissue is involved.  Cinzerling offers such sequence of its development:

a) development of inflammatory focus

b) reproduction of pathogen

с) spreading infected edematous fluid through the pores in the next few alveoli.

               In the alveoli serous exudate is formed with a large number of fibrin, in the bronchioles and bronchi mucus is accumulated, which causes their obstruction and appearance of atelectases. Finally, this leads to the formation of pathological changes in the form of focal (in particular, confluent), segmental, lobar, interstitial lesions, involvement in the pathological process of the pleura, lymph nodes (increasing).

              At any of these forms of pneumonia all the structural elements of lungs are involved in the pathological process greater or lesser, so in the diagnosis the predominant lesions of the parenchyma or interstitium are indicated. For example, a focal pneumonia (the most common form of pneumonia in children 1 year) indicates a lesion of the parenchyma and bronchi. It is inconceivable that in this disease have remained intact vessels, intraalveolar septums, lymph nodes, etc. Changes in the bronchi, bronchioles (ventilation violation), swollen interalveolar septums and interstitial tissue (diffuse disorders) impede gas exchange between blood and alveolar air. Exception from gas exchange of alveolars, sub-segments, segments, lobes (distribution  violation) contribute to the development of respiratory hypoxemia.

                  With the participation of interoreceptors the organism through the respiratory centers of the child reacts to the last increase in respiratory rate in order to eliminate hypoxia. However, the increase in respiratory rate oт 60% leads to a decrease in the depth of breathing in 30%, resulting in an increase in pulmonary ventilation only on 15%. In severe forms of pneumonia, when the respiration rate increases in 2-2,5 times the depth of breathing and lung ventilation are acutely reduced. However, the oxygen demand increases significantly with increasing body temperature, increased metabolism especially at the expense of activity of the sick organ (lung) and supporting muscles. Lack of blood arterialization is compensated by increased cardiac work, particularly right heart. Heart output and minute circulation volume are increased. All of this causes an acceleration of blood circulation in the lungs, frequent contact with lung tissue and improvement of the blood arterialization.

                However, with further progression of the pathological process in the lungs and prolonged rise of pressure in the pulmonary circulation, metabolic changes occur in the heart muscle, which causes its degeneration, diminished activity. This leads to disruption of blood circulation in the lungs, in hemo-and lymphostasis with the development of circulatory hypoxemia . That’s why a severe form of pneumonia is a disease with respiratory-heart failure.

                Further deepening of the pathophysiological and pathological changes in broncho-pulmonary system contributes to the violation of oxid reduced processes, which leads to the accumulation of incompletely oxidized products of metabolism in the body, increasing the content of pyruvic and lactic acids, the acidosis shift of acid -alkaline balance.

Oxygen uptake in tissues is stoped (hemical and anemic hypoxemia), hypoxia develops with expressed severe clinical manifestations. At hypoxemia cyanosis is characteristic, at hypoxia – ashy-gray color of skin. Phenomena of hypoxemia (and all its 3 phases) results in a disturbed external respiration (the basis of the pathogenesis of pneumonia), and hypoxia – internal respiration.

                 As a result of hypoxemia and hypoxia, changes occur in all types of metabolism (protein, lipid, carbohydrate, water and electrolyte), the total  enzymopathy appears, polyhypovitaminosis occures. Infection at pneumonia (exogenous toxicosis), on the one hand, and the adverse effect of the accumulated products of metabolism (endogenous toxicosis), on the other hand, lead to functional and sometimes to organic changes in all organs and systems, as well as to disorders of immunologic homeostasis. It is clear that the above cascade of profound change is absent in the mild forms of the disease and rare in children older than 2 years.

             An analysis of 323 child deaths due to pneumonia (data sections in the Ternopil region), representing 37% of autopsies over the past 5 years, found that from this disease children die mostly under the age of 1 year (97%), during the first week – 66% of newborns. In the children up to 1 month, pneumonia is often a major illness (79%), rarely developed as a complication of other diseases (21%). In children older than 1 month pneumonia as the main disease occurs in 17%, as a complication – in 83% of cases.

             Neonates primarily have aspiration pneumonia (53%), influenza (22%) and result of pneumopathy (14%). In children older than 1 month bronchopneumonia develops in 95% of cases, lobar – 3,5%, interstitial – in 1,5%. It is dominated polysegmental (43%) and large-focal (27%) pneumonias. The nature of inflammation iewborns prevail serous hemorrhagic pneumonia, among older children – fibrinous and purulent.

         In stillborns and premature infants pneumonia mostly is caused by Gram-negative flora (70%), in the term infants Gram-negative and Gram-positive flora is found equally frequently.

                             

Scheme of pathogenesis                             

         The penetration of patogen in lung tissue→ the formation of an inflammatory focus→ hypoxemia→respiratory failure→ respiratory acidosis→hypercapnia→ decreased activity of respiratory enzymes. Hypoxia (a respiratory acidosis associated with metabolic)→ hypercapnia→ violations of all types of metabolism→ decrease in cellular and humoral immunity.

 

 

                        

  CLASSIFICATION OF ACUTE PNEUMONIA

 

Types 

– focal

– segmental (mono- or polysegmental)

croupous

– interstitial

Localization

Lung, lobe, segment, one side or both side

Forms

– community-acquired, hospital (nosocomial)

– at perinatal infections

– ventilate-associative

– aspiration

– at immune deficiency

Severity

Mild, moderate and severe (severity is in accordance to clinical features and presence of complications)

Complications

Lung complications: pleurisy, lung destructions, pneumothorax etc.

Out of lung complications: infection toxic shock, cardiovascular failure, DIC-syndrome, respiratory distress syndrome of adult type

 

                  

                                                   CLINICS

 

                     Clinical manifestations of the disease in infants depend on sex (mainly boys are sick, they have also increasingly concentrated fatal pneumonia), age (in younger children it is more severe and more frequently fatal), premorbid state of the organism (severe pneumonia takes place on a background of prematurity, malnutrition, rickets, exudative-catarrhal anomalies constitution, etc.), the nature of agent (staphylococcal pneumonia is always severe, pneumococcal – easier). In early childhood pneumonia mainly developes on the background of ARVI, measles, pertussis and other diseases, so the course and severity of disease also depend on the nature of the virus (severer due to respiratory syncytial, influenza, measles) or bacterial (staphylococcal septicemia) infections. All of the above determines the individual peculiarities of pneumonia.

                  For most children, onset is gradual with manifestation of respiratory symptoms (sneezing, runny nose, dry cough), a slight increase in temperature, slight perioral cyanosis with anxiety, pallor of skin, lethargy, sleepiness, negative reaction to his surroundings. Then signs of external respiration disorders occur: frequency and shallow breathing, a violation of its rhythm (irregularity, arrhythmia, periodic apnea), shortness of breath, change in the ratio of respiration and heart rate (normal – 1:3,5-4) to 1:2, 5 – 1, 5.

              Objectively it is marked retracted compliant areas of chest during breathing, the participation of auxiliary muscles. Percussion: shortness or dullness of percussion sounds above the lesion. Auscultation: the presence of localized moist or dry wheezes. The physical pattern depends on the type and severity of pneumonia.

 

                      

                                   Points of comparative percussion

 

                  

                                                    Auscultation

 

                It must be remembered that in extremely serious condition cardiovascular failure may develop, characterized by acute increase in the frequency of heart contractions and frequent apnea. In such situation the ratio of respiration and heart rate will be “normal” – 1:4.

                We need to pay attention to the characteristic sing for  pneumonia in premature and newborn (50%): selection foamy mucus from  mouth and nose

(Kravets symptom), synchronous to the breathing head motion on the pillow top to bottom (the first month of life), thickening of skin folds in chest on the side of lesion.

               Later occur: pale skin, cyanosis, in severe cases – cyanotic marbling and grey colour of the skin. It is observed the tension and swelling of the nostris, shortness of breath has “grasping” nature. Breathing is increased in 1,5-2-2,5 times compared with the norm, apnea occurs several times a minute, the ratio of respiration and heart rate – 1:2-1,5. Thorax is emphysematous, barrel, percussion first shows boxed sound, later – a shortening in the area of confluence of small foci of affected segments. The presence of disseminated small foci of inflammation of the lungs may not cause changes on percussion because they are surrounded by emphysematous changed parts of the lungs.

 

                         DIAGNOSTIC CRITERIA OF PNEUMONIA

 

Clinical             Increasing of  body temperature above 38°C, hyperthermia

                          during 3-5 days and more; dry cough at first, then

                          moist; signs of intoxication and respiratory

                          failure; at palpation  increased voice fremitus,

                          at percussion over the affected area of lung

                          a shortened tympanitis, at auscultation –

                          hard breathing, first dry, then moist sonorous

                          small and medium bubble wheezing, possible crepitation

                          over the size of lesions, enforced bronchophonia.

 

  

 

X-Ray                 Infiltrative shadows in the form of foci of different

                            size and intensity, darkening of one or several segments, lobe or

                             several foci.

 

                   Diagnostic criteria of acute destructive pneumonia 

 

Clinically     Manifested intoxication, focal physical  symptoms (increased voice

                     fremitus over the area of destruction, shortening of percussion sounds,

                     hard breathing) at infiltrative-destructive form.

                     Intoxication, respiratory, cardio-vascular insufficiency, disseminated 

                     wheezing at abscess form.

                     Syndrome of internal thoracic intensity (marked paleness of skin,

                     Cyanosis of nose-labial triangle and acrocyanosis, shallow breathing,

                      dyspnea, tachycardia), position on the sick side, the backlog of

                      respiratory excursions on the side of destruction, percussion –

                      shortening of the sound, auscultation – relaxed breathing or its

                      absence at lung-pleural forms.

 

  

X-ray            On the background of infiltration of lung tissue appearance of local

                      small round air formations (infiltrative – destructive form).

                      On the background of polysegmental infiltration presence of

                      circular formation with expressed shadow, later – cavity formation with

                      the level of fluid (abscess form).

                      Simultaneously with pulmonary infiltration parietal shadow in the area

                      of the sinuses (pyothorax).

                       The presence of air above the horizontal level of the liquid,

                       displacement of the shadow of the mediastinum, enlargement of

                       intercostal intervals (pneumoempyema).     

 

                 For pneumonia, which occurs in children 1 year of life, there are not characteristic percussion changes, but are noted increased respiratory noises, crepitation  and small bubbling rales. Segmental, lobar pneumonia are characterized by shortening of percussion sounds and bronchial breathing. At atelectasis, except shortening percussion sounds, breathing is weak or absent. This clinic shows the need for exclusion exudative pleurisy (radiologically).

                For putting the diagnosis of disease it is very important X-ray examination – limited homogeneous shadowing within one segment (or segments) of the lungs is characteristic for pneumonia in children older than one year. The same changes are observed at atelectasis, agenesia, hypoplasia of the lungs. At pneumonia often occurs the infiltrative enlightenment in the center and the level of liquid in it (abscess). Pneumonia in young children at X-ray is accompanied by soft, small (1-3cm), round infiltrative shadows on the background of intensive, stranded lung pattern (bronchitis, peribronchitis). Net-stranded or stranded spotted lung pattern is characteristic for influenza and measles, pneumonia, and sometimes for the interstitial forms of staphylococcal pneumonia.

 

                         X-ray examination

 

 

For illustration we present an excerpt from the medical card N 8775.

 

    Girl M., 3,5 months, was hospitalized in the pulmonary department with the acute bilateral bronchopneumonia viral-bacterial etiology, severe course with the obstructive syndrome during the crisis period, RF II st.; Iron-deficient anemia, alimentary-infectious origin moderate form.

Complaints on a dry cough, shortness of breath, anxiety.

Anamnesis of the disease: the disease occurs acutely 4 days before hospitalization, after contact with patients with ARVI of family members. The girl fell appetite, started to cough, body temperature increased to subfebrile. Over the next two days the state progressively deteriorated: the body temperature remained high (despite antipyretics, which his mother gave the child), coughing became more often and severe, the girl refused to eat, short of breath occured and began to grow. This has forced parents to visit a doctor, and the child was hospitalized at the District Hospital. In the District Hospital was during 3 days. In connection with the further deterioration was tntered to Regional Hospital.

Anamnesis of life: a child of II  term normal pregnancy, II normal childbirth. Weight at birth – 3100g, body length – 50cm. Cried at once, breast feeding from the 1-st day, sucked actively. Umbilical residue dropped on the 4-th day, the wound healed at the 6-th day; at the 7-th day the girl in a satisfactory condition was discharged at home.

                       Breastfeeding lasted approximately 1.5 months, from 1.5 months of age (due to mother hypogalactia) the child was transferred to artificial feeding by cow’s milk, first diluted (1:1 – 3 weeks, 2: 1 – 2 weeks). Before the disease, she received whole cow’s milk. Juices and fruit purees were introduced after 3 months. (Gets occasionally no more than 1 teaspoon a day).

Objective status: status of girls at entering to TRH was severe, which led to her hospitalization in the intensive care unit. The condition was due to respiratory failure and intoxication.

Normostenic, a satisfactory nutritional status. Skin was pale with a gray tinge, cyanosis of the lips and nasolabial triangle, increased by coughing and crying. Subcutaneous fat developing is satisfactorily (the thickness of skin folds at abdomin – 1,5cm), distributed evenly. There are palpable single back and front neck lymph nodes (2-3 in each group), their diameter – up to 5mm, they are soft-elastic, not soldered to the surrounding tissues, mobile, not painful. The head is round, without deformation, large fontanellae (2 x 1, 5cm) at the level of the skull bones, the edges are dense, smooth.

          The boundaries of relative cardiac dullness: the right-parasternal line, upper – II rib, left – 2cm outward from the left sternocleidomastoideus line. Cardiac rhythmical tones are slightly weakened, heart rate – 152 per 1 min. Soft systolic murmur is auscultated above the apex of the heart.

         Thorax somewhat blown, symmetric. Support muscles are involved in the act of breathing, nostrils are tense. At percussion over the surface of the lungs it is determined  clear pulmonary sound with slightly bandboxing , the sound is shortened paravertebrally. At auscultation – hard breathing, in the lower parts of both lungs fine bubbling moist rales in large quantities are listened. BR – 66-68 per 1 min, extended exhalation.

          Abdomen is slightly distended, palpation is not painful, the lower edge of the liver is 2 cm under the costal arch, soft, elastic, smooth. Feces – 2 times a day, mushy, without pathological impurities.

X-ray of lungs: at both sides in the medial areas there is focal infiltration of the lung tissue, in other areas – an increase of pulmonary pattern against the background of acute inflation of the lungs. The roots are low structured, infiltrated.

        General blood analysis: Er. – 3,02 x1012 / l, Hb75 g / l, CI 0,7; Leuc. – 8,9 x109 / l, e-1, b -10, s -47, l39, m – 3, ESR – 3 mm / h.

Analysis of urine, feces, coprogramm – without pathological abnormalities.

Criteria of diagnosis of pneumonia in the child:

1. Signs of respiratory distress (shortness of breath, swelling of the nistrics, cyanosis

    of nasolabial triangle, participation in the act of breathing of axillary musculature.

2. The symptoms of intoxication.

3. Local changes: a shortening of percussion sounds paraver

    tebrally, hard breathing, in the lower parts of both lungs – fine

    bubbling moist rales.

4. Radiological findings: on both sides in the medial areas infiltration of the lung

    tissue.

5. general blood analysis: leucocytosis, shift to the left.

Treatment: Ampicillin and Gentamicin intramuscularly, Fluimucil, Aktiferin, vitamin A, Linex, infusion therapy (saline, glucose, aminophylline – 2,4%, vitamin C, Riboxin), massage of the chest in the drainage position, stimulation of coughing.

The perculiarities of pneumonia in the child: the disease was developed on the background of anemia caused by malnutrition.

Type of pneumonia was little focal (bronchopneumonia), which is characteristic for early childhood. There was also obstructive syndrome and severe intoxication.

                       Segmental and lobar pneumonia are more common in children of 2-3 years. Characteristic for them are acute start, severe disturbance of the general condition, hyperthermia. Cough initially is absent or negligible, expressed pain in the right iliac region, vomiting, shortening of percussion sounds, up to absolute dullness, expressed bronchophonia. Shadowing of segment (segments) and lobe on  X-ray confirms the diagnosis of pneumonia and eliminates the acute abdomen. Without treatment the course is cyclical.

                          

                                      Right sided lobar pneumonia

                   

                              Right sided polysegmental pneumonia

 

                     

 

X-ray of the chest in the front projection at left-sided upper staphylococcus pneumonia: On a massive shadowing in the upper lobe of left lung there are seen multiple round of enlightenments – cavities.

 

               

Radiogram of the chest in front projection with focal interstitial pneumonia: the background of a strengthened and strained lung pattern in both lung fields, predominantly in the right, there are visible focal shadows of different sizes.

 

Radiograph of the chest in front projection with the focal

pneumonia: in both lungs are visible clearly delineated shadows

 diameter of 1-2 cm.

 

Roentgenogram of chest in a front projection at croupous upper right-sided pneumonia: in the right upper lobe there is defined shadowing, limited by interlobar pleura, the volume of the lobe is not reduced, the bronchial tree in it is transparent.

 

Thermogram of the back surface of the thorax with croupous right-sided pneumonia: in the right lung there are determined  confluent foci of hyperthermia (yellow).

 

          The diagnosis of pneumonia is justified by the following criteria: respiratory failure, presence of symptoms of intoxication, the local percussion (shortening) and auscultatation (crackling or wheezing fine rales) changes, tension and swelling of the nostris, involving the sternum, intercostal spaces, over-and subclavian areas; participation in the breath of abdominal press; focal, segmental, lobar infiltrative shadows (radiologically), neutrophilic leukocytosis and a shift to the left, increasing of ESR, respiratory or mixed acidosis.

 

                 Intrauterine and neonatal pneumonia

  

     Intrauterine and neonatal pneumonia differ in clinical manifestations of pneumonia in older children:

1) it is possible to identify the relationship between changes in intrauterine fetal development and inflammation in the lungs, the disease may be a manifestation of sepsis or the first is the respiratory distress syndrome and later developed pneumonia followed by sepsis,

2) for younger (in days) and maturity of the child, bright manifest forms of pneumonia are rear, and therefore their diagnosis increases the value of supporting research methods, 

 3) a destructive form of pneumonia tend to occur in full-term children with septic focus of the pathological process,

4) relatively long disease duration (3 weeks) and the recovery period (up to 4-6 weeks). Imunoglobin G and the partial pressure of O2  are visibly reduced, the hypovitaminosis and anemia are observed.

 

                           Destructive pneumonia

 

          The features of destructive pneumonia (often staphylococcal origin) are: expressed intoxication, gray colour of skin, neurotoxicosis, respiratory and cardiovascular failure, severity of disease, significant changes of all organs and systems, meteorism, significant neutrophilic leukocytosis with left shift, increased ESR, anemia. If acute pneumonia lasts more than 6 weeks, according to the  classification, it is protracted pneumonia. For destructive pneumonia, this criterion is not relevant, since the acute phase may last for 8 or more weeks. More specific manifestations is the presence of pneumatocele (Bullas, thin-walled air cavities in the lungs, which are determined radiographically), which can swell up to large sizes, lung abscess, pneumothorax, pneumoempyema, subcutaneous emphysema and mediastinal emphysema, staphylococcal enterocolitis.

 

Pneumoempyema: A–in standing position, B–in lie position, C–in lateral position.

 

 

 

 

Pneumoempyema: A–before treatment, B–a week later, C–after treatment.

 

 

 

      

 

      Pleurisy

 

 

 

Destructive pneumonia with abscess.

   

Abscess of right lung.

 

WHO for primary health care system suggests using such diagnostic test: breathing more than 50 minutes per 1 minute indicates pneumonia, more than 70 per 1 minute –   the severity of its course. Identify the causative agent is problematic in connection with the imperfection of modern methods of investigation. 

 

 

Clinical classification of acute pneumonia provide the type, severity of disease.

Type of disease is predominantly determined by X-ray:

Ø focal bronchopneumonia

Ø segmental pneumonia;

Ø lobar pneumonia;

Ø interstitial pneumonia.

The severity is determined by the severity of clinical manifestations and the presence of complications.

               Mild form of disease is characterized by a slight violation of general condition, a moderate increase of temperature (not more than 38,5°C), respiratory insufficiency II degree, blood gases at rest are not changed.  At a mild course of the disease tere are changes in  the lungs and no changes in the other organs and systems.

 

                 Severe pneumonia in children is characterized by changes both of the bronchopulmonary system, as well as other organs and systems. And, sometimes clinically the disorders of the central nervous system, heart, digestive organs are the main. For example, the doctor examines the patient, who expressed hyperthermia (40-41°C), depression of consciousness or loss of consciousness, seizures. And only the lumbar puncture showed that the changes in the spinal liquid are absent, and later  examination of  the patient define all symptoms of pneumonia.

    Therefore it is desirable to specify a diagnosis not only the severity of the disease, but also a meninoencephalitic syndrome (hypoxic encephalopathy). The presence, along with pronounced signs of respiratory distress, changes in the cardiovascular system (small frequent pulse, expanding the borders of the heart, deafness tones, systolic murmur, may be swelling of the neck veins, ECG changes) indicate presence of  myocardial hypoxia and pronounced cardiovascular syndrome. Dyspepsia (vomiting, frequent liquid feces, meteorism) indicate the intestinal syndrome. Acute hypotension, general cyanosis, pulse, which is not defined or thready, heart rate, which is not countable, vomiting, diarrhea show the adrenal insufficiency syndrome.

 

Acute moderate pneumonia is accompanied by a intermediate manifestations compared to the above clinic. It is marked by disturbed general condition, respiratory insufficiency II degree, manifested changes in other organs and systems, but they do not predominate over the symptoms from the lungs.

Standard classification of acute pneumonia differentiate acute course (during 6 weeks) and protracted (over 6 weeks). But this logic breaks down: acute pneumonia caot be both protracted. Therefore, during her periods should be distinguished: 1) initial, 2) the clinical manifestations, 3) regression and 4) recovery.

 

The differential diagnosis of the disease is carried  primarily with bronchitis, bronchiolitis, acute respiratory viral diseases. 

 

                        Scheme of differential diagnosis of acute pneumonia

Characteristic for pneumonia

 

Non characteristic for pneumonia

Body temperature higher 38°C more than

3 days

 

 

Cyanosis

Hard breathing

Unproductive dray and moist cough

Dyspnea with obstructive syndrome

Local signs:

local moist rales, weak or harsh breathing, intensive bronchophony,

short percussion sound

 

Neutrophyle  leucocytosis more than

10×109/l, ESR more than 20 mm/h

Body temperature lower 38°C

Body temperature higher 38°C  up to

3 days

 

Absent

Absent

May be different variants

Absent

 

 

Disseminated dry and moist rales

 

 

Normal hematological features

 

 

 

          Differential diagnosis of focal pneumonia, bronchitis and bronchiolitis

 

 

 

Diseases

Functional changes in lungs

X-ray changes in lungs

Percussi

on sighs

Type of

breath

Rales

Root of

the lungs

Vascular

pattern

Local focal shadows

Focal pneumonia

Lung sound with box inflection

Harsh, focally weak with bronchial inflection

Local fine

moist or crepitation

Widening

nonstructive

on both sides or on the side of lesion

Mostly

intensive

on the

side of lesion

Different size and

density

sometimes

confluent

Simple bronchitis

Lung sound with box inflection

Harsh

Dissemi

nated moist and dry rales

Widening

nonstructive

on both sides

Intensive

on the

both sides

Absent

Obstructive

bronchitis

Bandbox sound

Harsh

Dissemi

nated dry rales

Widening

nonstructive

on both sides

Intensive

on the

both sides, swelling of lungs

Absent

Bronchioli-tis

Bandbox sound

Harsh

Dissemi

nated moist fine  rales

Widening

nonstructive

on both sides

Intensive

on the

both sides, sharp swelling of lungs

Absent

 

 

              Segmental pneumonia must be differentiated from segmental

                        acute pulmonary edema at ARVI.

 

                  Unlike pneumonia, segmental edema occurs more frequently in children older than 2 years. The characteristic feature of it is the disparity between the clinical picture of X-ray changes. Respiratory failure is rare. Physical symptoms are not pronounced. Radiological examination revealed massive homogeneous shadows within one, rarely several, in segments of the lungs, usually with a localization within the II-III or IV-V segments of the right lung. Unlike pneumonia, with repeated X-ray examination after 3-5 days, these shadows disappear and on their place there is only an intensification of the vascular pattern. The picture of blood in patients with segmental pulmonary edema is not changed and corresponds to the same virus infection: leukopenia, lymphocytosis. Normal or slightly elevated ESR.

                  Incorrect diagnosis of acute pneumonia leads to unnecessary prescription of antibiotics, unreasonably long delay of the child in hospital.

 

 

                                         TREATMENT

 

                  Treatment of the disease is always complex and aims to eliminate the causative agent, to liquidate oxygen deficiency and toxicosis, to restore function of organs and systems and increase resistance.

                 Therapeutic and protective regime is required for the inflammatory process subsided, and prevention or minimizing hypoxemia. The successful treatment is nursing a patient with participation of mother. The excitation and crying are significant physical activities that enhance oxygen deficiency. Therefore, it is necessary that the diagnostic and therapeutic procedures were as forgiving (to hold in the intervals between sleep). It is necessary to eliminate bright light, noise, provide frequent changes in body position in bed with head up. Wards for the sick children with pneumonia, should have sufficient space (at least 6.5m2 per child). To prevent reinfection it is required separate boxes, bright, ventilated, with frequent (4-5 times a day) ultraviolet irradiation. Temperature in the ward – 18-20°C, for newborns –

22-24°C.

                                           

 

                     Feeding the child must be gentle and easy to digest. The best is breath milk, even the donor milk, in its absence must be used the adapted milk formulars.

In the mild, and occasionally moderate, the disease volume of food and the intervals between feedings should be the physiological, in severe cases- in the first days of feeding expressed breast milk (to limit physical activity) through 2-2,5 hours – in small doses (up to 50% of normal) because appetite extrimely reduced or absent. Of course, the kid himself regulates the quantitative aspect of feeding depends on the severity of the pathological process.

                    Complete denial of food is an indication for parenteral nutrition. Once markedly reduced toxicity phenomenon and respiratory failure, the appetite is restored and the child goes to the normal (end of I and the beginning of the II week of disease). The need for vitamins increases in 2-5 times, and it should be satisfied (preferably enterally). Additional fluid loss, on the one hand, and the risk of pulmonary edema (severe course), on the other hand, is the basis for thorough correction with the help of rehydration therapy. We must remember that a child should not receive less than 150 ml / kg. He gets it while eating and drinking

(vegetable-water, apple skins-water, carrot-water, rice-water, 5% glucose solution, Oralit), as well as infusion therapy. In milder forms of pneumonia, usual diet and treatment provide the child with all the necessary ingredients of food, because a mechanism of self-regulation is not distorted.

 

                 Aero-and oxygen therapy are simple and effective in tretment or prevention of hypoxemia. This requires periodical toilet of nose, sucking the mucus from the pharynx (always before feeding), ventilation the ward, walk in the fresh air with the principle of gradualism (at environment temperature 17-22°C – maximally, perfectly – around the clock). Older childreeed to learn to release mucus from the nose. Pulmonary office should be boxed, have pleasure chamber used in bad weather. Outdoors child with this disease calms down, sleep, breathing becomes not so frequent, cyanosis disappears. In severe pneumonia patient required a 30-minute oxygen supply (usually through a catheter, a tent, mask) 3-4 times a day to improve the breathing rhythm, reduction or disappearance of cyanosis, to improve the general condition. Local action for edemata nasal mucosa (Sol. Norsulfazoli 0,8% – 15 ml; Furacilini 0,01 and Dimedroli 0,05; Ephedrini 0,2; Sol.Adrenalini hydrochloridi 0,1%,  10 gtt. MDS –  2 drops in each nasal passage before breast-feeding) improves the ventilation function of the upper respiratory tract.

 

           At severe pneumonia, as a rule, there is marked respiratory and circulatory hypoxemia, which clinically are manifested by respiratory failure and cardiovascular syndrome. Therefore, in such cases, treatment begins with a slow introduction of a cardiac glycosides (Strophanthin solution  0,05% or 0,06% Corglikon solution 0,012 ml / kg) in 20% Glucose solution (5 ml / kg) with Cocarboxilaze (5 mg / kg ) and vitamin C (100-200 mg). Under these conditions there are disorders of  the microcirculation (especially in the lungs and heart) and blood rheology, which needs use of antiplatelet agents (Curantil), hemocorrectors (Reopolyglucine), anticoagulants (Heparin). Whilst the therapy is aimed to liquidate the cardiovascular insufficiency, its ultimate task – to eliminate the phenomenon of hypoxemia and the normalization of metabolic processes.

 

                Not only at severe pneumonia, but less at moderate, there is marked the phenomenon of toxicity, accompanied by hyperthermia and convulsions. Therefore it is needed the appointment of desintoxication therapy: Albumin, Plasma, Haemodes (intravenously, in the warm form,  5-10 ml / kg / day). To a great extent these qualities are inherent in Albumin, then – Plasma, then – Haemodes.

 

                  It is known that high temperature requires sharp increases in metabolism, oxygen demand, therefore, leads to accumulation of toxic metabolic products and the deepening of hypoxemia and hypoxia. Therefore, advisable to appoint non-specific anti-inflammatory drugs, Amidopyrine (1% solution), Analgine (25% solution – 0.25 ml / year); Lytic mixture (solutions of Aminazine 2,5% – 1 ml, Pipolphen 2 5% – 1 ml, Novocaine 0,25% – 4 ml) intramuscular injection of 0.1 ml / kg per injection. In weaky antipyretic effect of drugs at the presence of convulsive syndrome it should bt prescribed intravenously 20% solution of Oxibutirate sodium (100 mg / kg) , 0.5% solution of Diazepame  (intravenously or intramuscularly 0.5 mg / kg), 0, 25% solution of Droperidoli (0.5 mg / kg). Do not forget about the methods of natural decreasing of temperature: ice pack on head, on the area of liver, large vessels, and intestinal water enema at a temperature of 18-20°C, intravenous solutions at a temperature of 10-15°C.

 

             With all the severe illnesses in young children, especially pneumonia, there is a disturbance of acid-alkaline balance (acidosis). It is known that the enzyme activity in the body depends on the pH. The lower is pH, the lower is the activity of enzymes, the lower are the metabolic processes, the more distorted responses are from the organism to the introduction of therapeutic concentrations of drugs. There is no doubt that treatment (though it was directed at other parts of the pathogenetic changes) increases the pH, but the direct antiacidosis drugs must also be entered: 4% solution of sodium intravenously droply  3 ml / kg (moderate), 5 ml / kg (severe form) in the 2-3 receiving, in order to prevent alkalosis. Hormone therapy is rare (only in severe pneumonia) in large doses (2-3 mg / kg Prednisolone), but short course (3-5 days) and the simultaneous removal without complying with the principle of gradualism.

 

                               Antibiotic therapy

 

                Antibiotic therapy is effective only together with pathogenetic treatment. It is assigned after putting or even the predisposition of the diagnosis of acute pneumonia, and the duration and intensity depend on the severity of the process and the presence of complications. Tentatively it looks like this: mild course – 5-7 days, moderate – 10-14 days, severe – up to 3 weeks, complication (abscess, pyopneumothorax, empyema) – not less than 4 weeks.

 

             Due to the fact that in most cases the cause of pneumonia is cocci (pneumo-, streptococci and staphylococci) the complex therapy includes Penicillins (Benzylpenicillin, Oxacillin, Methicillin, Dicloxacillin, Ampicillin, Carbenicillin, Azlocillin, Mezocillin etc.). Their dose at mild course is 50-80 thousand / kg / day, moderate – 80-100 thousand / kg / day, severe – 100-150 thousand / kg / day, at complicated pneumonia – 250-500 thousand / kg / day, introduced into 3-4 injections.

 

               If at mild acute pneumonia, there is assigned one antiiotic medication, at the moderate – sometimes two, at a severe – two, and at the complications of pneumonia – obligatory two drugs, sometimes three (one – intravenously, the second – intramuscular, the third – orally) .

       Effective is a combination of Penicillins with Aminoglycosides (Gentamicin, Sizomicin, Brulamicin, Tobramicin – 2-4 mg / kg / day in 2 injections), Cephalosporins (Cefalotin, Cephalexin, Cefazolin – 50-100 thousand / kg / day intravenously, intramuscularly) , to a lesser extent – with Macrolides (Erythromycin – intravenously 20 thousand / kg / day, Oleandomycin – 25-50 thousand / kg / day, intramuscularly) or similar in mechanism of action of Lincomycin (30-60

mg / kg / day intramuscularly in 2 injection). Combination may be: Aminoglycosides and Cephalosporins, Aminoglycosides and Macrolides, Cephalosporins and Macrolides. Tetracyclines are appointed only after 10 yrs old, due to their toxic effects on the liver and the development of teeth.

 

             Other antibacterial agents are used less frequently: when drawing up individual treatment plan (Sulfonamides, Nitrofurans, Fuzidin, Chloramphenicol, etc.).

              Antistaphylococcus drugs are prescribed at destructive pneumonia when you can most likely think about staphylococcus etiology or after bacteriological confirmation. They are especially effective on the first week of the disease. They include: Antistaphylococcus Immunoglobulin   (not less than 35 IU / kg intramuscularly daily, № 3-4), Antistaphylococcus plasma (5-10 ml / kg daily intravenously, № 3-4). Native Staphylococcal Anatoxine (0,1, 0,5, 1 ml, 1 ml, 1 ml subcutaneously every other day N10), Staphylococcal Antifagine ( 0,1 ml, increasing daily by 0.1 to 1 ml, or every other day, subcutaneously prescribe simultaneously or separately in the period of regression of symptoms, but not earlier than 10 days after the introduction antistaphylococcus antibodies (Plasma, Immunoglobulin).

 

                    

 

                         

  Apparatus physiotherapy

 

                     Apparatus physiotherapy during the acute clinical manifestations of acute pneumonia is contrindicated. With the normalization of temperature, the elimination of respiratory and cardiovascular failure may be prescribed  diathermia (UHF, MHF, LHF), in the period of convalescence – electrophoresis (with dionini, calcium, vitamin C), UVT. The beneficial effect is from ozokerite applications on the abdomen (especially the liver) in the period of the regression of disease subsided (20 min, 40°C). The positive effect is comforting the child (falling asleep, reduced meteorism and improves the function of the liver and intestine.

                  Tendency to abscess formation, prolonged, severe course, the lack of effect of usual antibiotic therapy are the indication for the appointment of intraorganic electrophoresis with antibiotic (Ceporin, Azlocillin injected intravenously in saline solution with the addition of a single dose of aminophylline and heparin and with a simultaneous electrophoresis). Electrophoresis in this case is longer (30-40 minutes) from the usual methods (15-20 minutes).

 

   Electrophoresis

 MHF-therapy

 

 

Ultraviolet irradiation therapy

 

 

 

 LHF-therapy

 

 

 

                                    

 

 

   Apparatus for UHFtherapy «UHF 30-2»

 

The apparatus is intended for therapeutic effect on the patient by ultra electromagnetic waves of high frequency.

 

 

                                                                         

Laser therapy apparatus BTL-5110

 

Single-channel laser therapy apparatus that generates the red and infrared radiation, with an open modular system that allows to improve the device.

 

Ultrasound therapy apparatus BTL-4710 Sono Professional


              

 

A simple and inexpensive apparatus for combined physiotherapy BTL-4810S Combi Optimal, which provides two popular physical factors.

BTL-4810S Combi Optimal – Dual-two channel device (single-channel electrotherapy + ultrasound).                     


 

 

 

                            Etiologic antibiotic therapy

Age

Etiology

Medications of the first line

Alternative vedications

1-6 mths

Escherichia coli,

enterobacteria,

Staphylococcus aureus, rarely

Pneumococcus, Haemophilus influenzae, viruses

i/v, i/m:

ampicillin + oxacillin

amoxicillin + clavulanate, ampicillin + sulbactam

i/v, i/m:

cefazolin, ceftriaxone, lincomycin, carbapenem, cefuroxime,

cefotaxime.

All drugs may be introduced with aminoglycosides.

6 mths-6 yrs

Pneumococcus, Haemophilus influenzae, viruses

orally: amoxicillin, phenoximetylpenicillin, macrolides

Orally: amoxicillin + clavulanate, cefuroxime,

i/v, i/m:

ampicillin

Cephalosporins II-III generation

6-15 yrs

Pneumococcus

orally: amoxicillin, phenoximetylpenicillin, macrolides

Orally: cefuroxime, amoxicillin + clavulanate

i/v, i/m:

penicillins, lincomycin, cefazolin

6 mths-15 yrs

(pneumonia

complicated by pleurisy

or destruction

of pulmonary

  tissue)

Pneumococcus, Haemophilus influenzae, Enterobacter

i/v, i/m:

amoxicillin + clavumanat,

ampicillin + sulbactam

cefurokam

i/v, i/m:

 cefazolin

+ aminoglycosides, cephalosporins III generation, carbepenems.

 

 

Main antibacterial medications and their dosage for children

 

Medications

Oral

Parental

Ampicillin + sulbactam

augmentin, Amoxiclav

50mg/kg

100-150 mg/kg, i/m

Cefazolin (kefzol)

 

50-100 mg/kg,  i/m,  i/v

Cefalexin

30-40 mg/kg

 

Cefuroxime

 

50-100 mg/kg,  i/m,  i/v

Cefuroxime aksetil (Zinnat)

30-40 mg/kg, during feeding

 

Cefotaxime (claforan)

 

50-100 mg/kg,  i/m,  i/v

Ceftazidime (Fortum)

 

30-100 mg/kg,  i/m,  i/v

Ceftriaxone

 

20-80 mg/kg,  i/m,  i/v

Carbepenems:

Imipenem (Tienam) Meropenem

 

 

60 mg/kg,  i/v

 

Monobactams

Aztreonam

 

 

120-150 mg/kg,  i/v

Aminoglycosides

Gentamicin

Amicacin

Netromicin

Netilmicin

 

 

5 mg/kg,  i/m,  i/v

     15-20 mg/kg,  i/v 

     10 mg/kg,  i/v

     5 mg/kg,  i/m,  i/v

Fluoroquinolones

Ciprofloxacin (Ciprobay, Ciprinol)

Oflaxacin (Tarivid)

 

15 mg/kg

 

7,5 mg/kg

 

    10 mg/kg,  i/v

 

      5 mg/kg,  i/v

 

Macrolides

Erythromycin Clarithromycin (Clacid) Dzhozamizin

Spiramycin (Rovamicyn) Roxitromicin (Rulid)

 

40-50mg/kg

15 mg/kg

30-50mg/kg

0,5 mill.U/kg

0,3g

 

     40-50 mg/kg,  i/v

 

Preparations of other groups

Lincomycin

Clindamycin

Rifampicin

 Clotrimoxazol

 

Metronidazole

 

30-60mg/kg

20-40mg/kg

10-20mg/kg

8-10mg/kg

(trimetoprili)

22,5 mg/kg

 

10-20mg/kg,  i/m,  i/v

10-25mg/kg,  i/m,  i/v

10-20mg/kg,  i/m,  i/v

8-10mg/kg,  i/v

 

22,5 mg/kg,  i/v

 

                 Algorithm of medical care for a child with pneumonia.

 

1. Health-protective regime.

2. Antibiotic therapy.

3. Oxygen-therapy. The liquidation of respiratory failure and

   hypoxemia:

• a) To ensure free airway, optimization of ventilation (throwing head back, the

       output of the lower jaw forward – to prevent the retraction of the tongue)

• b) the removal of mucus from the nasopharynx, larynx, large bronchi – the

       stimulation of cough, aspiration of mucus, the appointment of stimulants, for

       thinning the phlegm (Bromhexine, acetylcysteine, mixtures based on the herbas),

       vibrating massage with postural drainage

• a) oxygen – inhalation of moistened 40-60% oxygen through a catheter, a mask, in

    oxygen tent for 30 minutes 3-4 times a day, at failure – ventilation.

4. Liquidation of cardiac, vascular insufficiency: cardiac glycosides (strophanthin

     0.05% – 0,012 mg/kg, ckorglikon 0.06% – 0,012 mg/kg) on 20% glucose solution

    (5 ml/kg) with Cocarboxilaza (5 mg/kg) and vitamin C (100-200 mg).

5. Liquidation of microcirculatory disorders and blood rheology disturbances:

     the use of antiplatelet agents (Curantil – 5mg/kg, Haemocorectors

     (Reopolyglucine 10 ml/kg/day, Heparin)

6. Liquidation of toxicity: albumin, plasma, Haemodesum 5-10 ml/kg/day.

7. Decreasing of hyperthermia: antipyretics of central action (analgine 25% – 0,25

    ml/year), lytic mixture (chlorpromazine 2,5% – 1 ml, pipolfen 2,5% – 1 ml,

     procaine 0,25% – 4 ml, i/m  0.1 ml/kg per injection), physical methods of cooling.

8. Correction of acid-alkaline balance: 4% solution of sodium carbonate (3.5 ml/kg in

     2-3 reception.

9. With the threat of ICS – syndrome: heparin 200-250 U/kg/day in the stage of

     hypercoagulation, 50-100 U/kg/day in stage of hypocoagulation.

10. Immunotherapy of  directed action (at Staphilicoccal, Proteus, Pseudomonas

      pneumonia): hyperimmune plasma 5-15 ml/kg, immunoglobulin 100 IU N 3-5.

11. Stimulative Therapy: adaptogens of plant origin – Eleutherococcus, Ginseng

      echinacea, medicine – pentoxyl, dibasol, metacil in combination with vitamins.

12. Physiotherapy: UHF, electrophoresis, UVI, inhalation, microwave therapy.

 

                      COMPLICATIONS OF PNEUMONIA

 

TENSE PNEUMOTORAX

 

Pneumothorax is accumulation of air in a pleura cavity with the valvular mechanism of its receiption, wich makes increasing of pleura pressure with the following stipulations of collaps of lungs, by displacement of mediastinum in a healthy side and development of acute respiratory and cardio-vascular insufficiency on the type of cardio-pulmonary shock. At the simultaneous receipt in a pleura cavity puss together with air pyopneumothorax occurs. The reason of disease can be a breach in the pleura cavity of lungs abscess and staphyloccocus bulles, exydative pleurisy, empyema of pleura; tense mediastinum emphysema, asthmatic state, trauma of thorax which is accompanied by the closed damage of lungs.

                                       

  Clinic

At the acute form of syndrome  tension is sudden acutely, pallor of skin, sticky death-damp, sick seizes air by the opened mouth, frightened, breathing is hard, cold sweat , suffering face; cyanosis, with increases; a pulse is weak, threadlike, increased shallow hard breathing, arterial hypotension, hypoxic comma.

At the subacute form of syndrome there is slow progressive worsening of the state, pain in a thorax and in a stomach during breathing, sickly cough, increase of pallor of skin, cyanosis, sweating, shortness of breath, tachycardia.

A chest on a sick side falls behind in breathing, intraribs intervals are extended. Percussion sound above lungs is tympanic, in lower regions (in pyopneumothorax) is shortened, respiratory noises on a sick side are absent.

The tones of heart are displaced to a healthy side, tones of heart are muffled.

X-ray shows the depression of lung, absent pulmonary pattern, flat diaphragm,

level of liquid or total darkening in pyopneumothorax.

 

A classic anteroposterior view of the chest showing pneumomediastinum. The lifted thymic shadow above the heart is a typical presentation of pneumomediastinum. (From Vidyasagar D: Respiratory disease in the newborn. <IT+>In:<IT-> Holbrook PR (ed): Textbook of Pediatric Care. Philadelphia, WB Saunders, 1993, pp 551.)

 

Right sided pneumothorax


 

 


Right sided emphysema with displacement of mediastenum and heart to healthy side

 

Help on prehospital stage.

1.             To release from clothes.

2.             To give the promoted position of body to the child.

3.             Permanent  moistened oxygen through a mask.

4.             20 % solution of Oxybutirati sodium  50-100 mg/kg of mass  for one

                    dose intramuscular or intravenously streamly on 10-15 ml  of 10 %

                    Glucose solution .

5.             At fasty growth of cardio-vascular and respiratory insufficiency punction

                    of pleura cavity must be conducted: for destroying of air- the place of

                    punction is III-IV intraribs intervals on a front or middle of axillary line;

                    for the delete of liquid (blood, pus) – in IV-VI intraribs intervals on a

                    middle or back axillary line. A puncture is conducted on the overhead

                   edge of lowlised rib on a depth of 2-3cm after analgesia by 0,5 %

                    Novocaine solution . At valvular pneumothorax  Bylau drainage  is

                    imposed.

6.             Immediate hospitalization in the surgical unit.

 

Help on a hospital stage.

1.             Oxygentherapy with moistened oxygen through a nasal catheter -40 %

                     oxygen constantly.

2.             20 % solution of sodium Oxybutirati 100 mg/kg (0,5 ml/kg) of mass is

                    for one  dose of intravenously very slowly on 10 % Glucose solution

                    20 ml; or 0,25 % solution of Droperidoli 0,1 ml/kg of mass

                    intravenously streamly slowly on 10 % glucose solution  15-20 ml.

3.             Pleura punction (look on prehospital stage).

4.             Solution of Corgliconi  0,06 % or Strophantini 0,05 %  0,01-0,015 mg/kg

                      of  the masses (but not more than 0,3 ml) for one dose on a 10 ml of

                      10% glucose solution  intravenously streamly slowly.

5.             Cocarboxilazae 50-100 mg, 5 % solution of sodium ascorbinaty 2,0-5,0

                      ml, Panangini 0,5 ml per year of life intravenously streamly on 10 ml of

                     10 % solution of glucose in separate syringes.

6.             Infusion therapy for desintoxication – 10 % Glucose solution 10-15ml/kg

                     of  mass.

7.             Antibiotics.

 

                                           Acute abscesses of lungs

 

                    Destruction of lung parenchyma under the influence of pathogens and emissions of their enzymes leads to the formation of delineated foci of fusion of lung tissue in the form of cavities filled with purulent exudate and detritus, and sometimes containing fragments of the sequestered lung tissue.

                 Abscess formation in the lung develops in the presence of several conditions, foremost of which, besides purulent creating pathogenic organisms, are the violation of bronchial patency and local disorder of pulmonary circulation. On the mechanism of development there are distinguished bronchogenic (including aspiration), hematogenoembolic, post-traumatic and lymphogenous lung abscesses. The allocation of so-called para- and postpneumonic abscess is incorrect, because initial phase of any of lung abscess is inflammation of lung tissue, and therefore any genesis abscess is para- or postpneumonic.

                Moments predisposing to the development of lung abscesses are low immunity, weakening of the child’s body. Acutely affects the general resistance of the organism and thus contribute to the development of lung abscesses and infectious diseases, primarily such conditions as epidemic influenza, severe injury, blood diseases, hypovitaminosis, prematurity, hypotrophy. A major predisposing factor for the development of septic complications, including lung abscesses, is diabetes.

                 Lung abscess may be caused by various microorganisms and therefore are polyetiologic disease. An important role in the development of lung abscesses, especially in childhood, play pyogenic cocci, especially Staphylococci. These microbes emit a large amount of toxins and enzymes that contribute to necrotic and destructive changes in lung tissue. Some rarer causes of pulmonary abscess formation are streptococci, Klebsiella pneumoniae, Enterobacter, Pseudomonas aeruginosa, or their combination with Staphylococcus. In the past 30 years in the development of lung abscesses there was significantly increased the role of anaerobic infection, which most often detected in aspiration genesis abscess. Many patients have a combination of various microorganisms, and they may vary in different periods of the disease.

             In addition to the already mentioned division of the mechanism of development, acute lung abscesses are divided into simple (pus), and gangrenous. The latter include abscesses, containing parts torn away as a result of necrotic ihorosic inflammation of lung tissue, known as sequestration. In addition, abscesses are single and multiple, central and peripheral, unilateral and bilateral, uncomplicated and complicated. 

             The disease usually starts on the background of one or bilateral pneumonia, most commonly aspiration genesis or influenza. The clinical picture in the formative stage of purulent cavities in the lung is determined purulent resorbtion fever, which is based on three factors: suppurant factor, due to the presence of necrosis and melting of the lung tissue, a factor of resorption, resulting in absorption of the decay products of tissue and microbial metabolism, and loss factor, due to loss of protein with purulent discharge. The patients in this period have a high, sometimes hectic fever, chills, excessive sweating, signs of intoxication. Patients are often concerned about a dry cough, chest pain. Physical examination reveal larger or smaller area blunting percussion sounds over which the breath is weakened, and enhanced voice trembling. After breaking an abscess in the bronchus cough becomes wet, sometimes suddenly cough up a large amount of pus, often hemorrhagic sputum, after which the temperature may decrease.

            

                 The most severe and protracted are multiple (especially bilateral) and gangrenic abscesses. The latter most often become chronic or complicated by a breakthrough in the pleural cavity, haemorrhage and sepsis. In severe, progressive course and the ongoing decay and suppuration of lung tissue on a background of increasing intoxication functional disorders of the cardiovascular system, liver and kidneys arise, which with the progression of the disease may be replaced by organic changes in the internal organs, characteristic of the septic condition.

                    Pronounced loss of protein and electrolytes during the acute phase of inflammation with its insufficient compensation leads to volemic and hydroelectrolitic disorders, reduces muscle mass and weight loss. On this background, there may be swelling of the lower extremities.

              As the disease progresses and complications develop the purulent resorbtion fever replaces purulent resorbtion exhaustation. Typically, this occurs in children with extensive destruction of the lung complicated with pleural empyema. On the background of progressive hypoproteinemia patients lose weight and grow thin. High temperature is replaced subfebril or normal, that is a poor prognostic sign, indicates a acute decrease in reactivity.

               The suspection of the beginning of abscess formation in a patient with severe pneumonia may be based on changes in clinical and physical examination data, but the main role in the diagnosis of lung abscesses has X-ray, which is preferably performed in a vertical position the patient. The appearance of one or more translucencies on the background of a homogeneous darkening of lung indicates the formation of single or multiple abscesses. The widely used term abscess pneumonia means only a certain period during the inflammatory process in the lungs and is not an independent nosological form. Later multiple small cavities may influent  into larger, in which, after coughing up sputum levels of the liquid begin to determine. To refine the localization of abscesses multi-axial fluoroscopy and radiography in frontal and lateral projections must be performed.

        

 An acute abscess of upper lobe of left lung. Visible massive inflammatory infiltration

around the abscess cavity.

 

 

  An acute abscess of middle lobe of right lung.

 

  

   Empty abscess cavity in the S6 of the right lung. Thickening of the wall cavity is seen almost throughout the full length.

 

                    Lung abscess should be differentiated from tuberculous cavities, purulant cysts,  abscess of bronchiectasis and cavitary form of lung cancer. Important role has bronchoscopy with biopsy, allows to exclude the presence of a foreign body, tumor of the bronchus, identify signs of specific inflammation in the bronchi, to obtain material for morphological and bacteriological studies.

                     Very often during the development of the abscess on the periphery of the lung there are difficulties in its differential diagnosis with encysted pleural empyema and pneumoempyema. Sometimes it is very difficult to determine where is the purulent cavity: in the lung or pleura, especially when these cavities are numerous. If on the multi X-ray scopy the shadow of the visceral pleura or the edge of the lung are seen, the presence of empyema may be probably excluded. Spherical or slightly oval form of the cavity is an evidence of lung abscess, elongated in the caudocranial direction –of  empyema. At empyema cavity width at low of the pole is always greater than that of the upper. The walls of the abscess cavity approximately have the same thickness, whereas the medial wall of the empyema cavity formed by the visceral pleura, usually thinner than the lateral. Internal contours of wall abscess are hilly and rough. At the massive destruction of lung internal boundary of encysted empyema cavity may not be the visceral pleura but destroyed and distorted lung parenchyma. The characteristic radiological signs such abscessempyema is unflat, eroded and thickened medial wall of the cavity. More precisely localize the cavity is due to a computer and NMR tomography.

 

  

 Encysted pneumoempyema. The rear cavity contours influent with the chest wall. Vertical cavity size significantly exceeds the horizontal.

 

 

                  To complications of acute lung abscesses include empyema, pleural pneumoempyema, pulmonary hemorrhage and septic conditions. The development of any complications greatly aggravates the course of the disease and worsens its prognosis. Outcome of acute lung abscess in addition to a full recovery with empting and scarring (obliteration) of purulent cavity, may be so called “Clinical recovery ” with the cleanup of well drained through the bronchi cavity, its stabilization and transformation on the thin-walled air cysts. Such a cyst in her relatively small size may be completely asymptomatic, but in adverse circumstances (activation of infection, the violation of cross-draining bronchi) in it may appear fluid and cause relapse of suppuration. Less favorable development is the chronical inflammation and its progression with associated complications leads to death.

 

                       Prevention of pneumonia in children

 

                     Prevention is the rational  feeding, active treatment of diseases, promoting the appearance of pneumonia (prematurity, malnutrition, rickets, birth trauma, anemia, abnormalities of the constitution, ARVI, etc.).

 

Primary. Nutrition, strengthening of the child, active treatment of diseases, leading to the pneumonia.

Secondary. Clinical supervision for convalescents during the year, restorative therapy 2-4 weeks after discharge from hospital and dynamic monitoring (paying attention to the nature of repeated respiratory infections); chest X-ray in the dynamics according indications.

 

 

        Emergency therapy of 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.

 [Zilberg P., 1989].

 

 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 iewborn

 

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.

 

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