Acute bronchial obstruction

Obstructive disorders in the lower respiratory tract occur as a result of obstruction of air movement in the trachea at the level of the carina of the trachea, large and medium bronchi.

Pathological conditions and diseases accompanied by broncho-obstructive syndrome:

• bronchial asthma;
• acute or recurrent obstructive bronchitis;
• bronchiolitis;
• heart failure;
• chronic obstructive bronchitis;
• pneumonia;
• poisoning with phosphorus-containing substances;
• tumor lesions of the tracheobronchial tree.

In some cases (bronchial asthma, obstructive bronchitis), bronchial obstruction dominates the clinical picture of the disease, in others (pneumonia) it occurs latently, but has a significant impact on the course of the underlying disease and causes complications.

Pathogenetic mechanisms of bronchial obstruction:

• spasm of bronchial smooth muscles;
• swelling of the mucous membrane of the bronchial tree with possible transudation of edema fluid into the lumen of the bronchi;
• hypersecretion of mucus;
• purulent crusts blocking the lumen of the bronchi;
• collapse of the bronchioles due to pressure on them from the outside by inflated alveoli;
• bronchial dyskinesia.

In most cases, the formation of bronchial obstruction is caused by all mechanisms, but in each individual patient their proportion is not the same, which explains the diversity of the clinical picture.

In children of the first three years of life, hypercrinia predominates, while in older children, the bronchospastic component predominates.

The development of obstruction at the level of the bronchioles is manifested by expiratory dyspnea, high-pitched wheezing against the background of local weakening of breathing, and a pronounced disturbance in the gas composition of the blood.

Obstructive bronchitis and bronchiolitis

In most cases, obstructive bronchitis and bronchiolitis are caused by a viral infection combined with an allergic component. Respiratory syncytial virus, parainfluenza, and rhinoviruses are distinguished. Recently, the role of chlamydial and mycoplasmal infections has increased. Unlike obstructive bronchitis, bronchiolitis affects small bronchi and bronchioles. Bronchioles are infiltrated; patency is sharply impaired, as in an attack of bronchial asthma.

Obstructive bronchitis is typical for young children, bronchiolitis is typical mainly for children in the first months of life.

The disease begins suddenly and is manifested by hyperthermia, shortness of breath, and anxiety.

During examination, accessory muscles are involved in the act of breathing.

Percussion of the lungs reveals a box-like sound; auscultation reveals a large number of moist, predominantly fine-bubble rales.

A natural consequence of bronchiolitis is hypoxia (55-60 mm Hg), metabolic and respiratory acidosis. The severity of respiratory failure in bronchiolitis is determined by the Fletcher scale.

Acute Bronchiolitis Severity Scale

Criterion	0 points	1 point	2 points	3 points
Respiratory rate in 1 min	Less than 40	40-50	51-60	More than 60
Difficulty breathing	No	Slightly	Only when exhaling	When exhaling and inhaling MspSS (, 1
The ratio of inhalation and exhalation time	2.5:1	1.3:1	1:1	Less than 1:1
Involvement of accessory respiratory muscles	No	Doubtful	Moderate	Expressed

First aid for the treatment of acute bronchial obstruction syndrome is inhalation of salbutamol (2-6 years - 100-200 mcg, 6-12 years - 200 mcg, over 12 years - 200-400 mcg) or ipratropium bromide (2-6 years - 20 mcg, 6-12 years - 40 mcg, over 12 years - 80 mcg) using a metered-dose inhaler or nebulizer. It is possible to use a combined bronchodilator - ipratropium bromide + fenoterol (up to 6 years - 10 drops, 6-12 years - 20 drops, over 12 years - 20-40 drops). For inhalation of young children, a spacer or aerochamber is used. In case of increasing acute respiratory failure, hormones are administered (prednisolone 2-5 mg/kg intramuscularly or intravenously) and repeated inhalations of a bronchodilator (ipratropium bromide + fenoterol, ipratropium bromide) are performed. If inhalations are limited, 2.4% 4 mg/kg aminophylline is administered intravenously by slow jet stream over 10-15 minutes in isotonic sodium chloride solution. Oxygen therapy with 40-60% oxygen and infusion therapy are mandatory. In case of severe acute respiratory failure and ineffective breathing, tracheal intubation and auxiliary mechanical ventilation with 100% oxygen are recommended.

Acute attack of bronchial asthma

An acute attack of bronchial asthma is an acutely developed or progressively worsening expiratory dyspnea. Clinical manifestations: dyspnea, spasmodic cough, labored or wheezing breathing. An exacerbation of bronchial asthma is characterized by a decrease in the expiratory flow rate, manifested by a decrease in FEV1 (forced expiratory volume in the first second) and peak expiratory flow rate during spirometry.

The volume of therapy depends on the severity of the exacerbation.

Criteria for assessing the severity of an asthma attack in children

Signs	Mild attack	Moderate attack	Severe attack	Threat of respiratory arrest (Stofus аsthmaticus)
Physical activity	Saved	Limited	Forced situation	Absent
Conversational speech	Saved	Limited; individual phrases	Speech is difficult	Absent
The sphere of consciousness	Sometimes excitement	Excitation	"Excitement, fear, respiratory panic"	Confusion, hypoxic or hypoxic-hypercapnic coma
Respiratory rate	Breathing is rapid	Expressed Expiratory Dyspnea	Sharply expressed Expiratory Dyspnea	Tachypnea or bradypnea
Involvement of accessory muscles, retraction of the jugular fossa	Not clearly expressed	Expressed	Sharply expressed	Paradoxical thoracoabdominal breathing
Wheezing	Usually at the end of exhalation	Expressed	Sharply expressed	"Mute lung", absence of breathing sounds
Pulse rate	Enlarged	Enlarged	Sharply increased	Reduced
FEV1, PEFb%ot of the norm or the best values of the patient	>80%	50-80%	<50% of normal	<33% of normal
PO2	N	>60 mmHg	<60 mmHg	<60 mmHg
PaCO2	<45 mmHg	<45 mmHg	>45 mmHg	>45 mmHg

Algorithm for the treatment of a mild attack of bronchial asthma

Inhalation of a single bronchodilator medication using a metered-dose inhaler or nebulizer.

Drugs used

Salbutamol (short-acting beta ₂ -adrenergic agonist); single dose via inhaler 100-200 mcg, nebulizer - 1.25-2.5 mg (1/2-1 nebulizer).

Ipratropium bromide (M-anticholinergic); single dose via MDI 20-40 mcg (1-2 doses), 0.4-1 ml via nebulizer.

Combination drug ipratropium bromide + fenoterol; single dose 0.5-1 ml via nebulizer, 1-2 doses using MDI (50 mcg fenoterol + 20 mcg ipratropium bromide).

After 20 minutes, the patient's condition is assessed. The criteria for the effectiveness of the treatment are a decrease in dyspnea, the number of dry wheezes in the lungs, and an increase in the peak expiratory flow rate. If there is little positive dynamics, a repeat dose of the bronchodilator is prescribed; if there is no effect, the severity of the asthma attack is re-evaluated and the therapy is adjusted according to the condition.

Algorithm for the treatment of a moderate attack of bronchial asthma

1-2 inhalations of bronchodilators are administered through an inhaler or nebulizer: salbutamol 2.5 mg (2.5 ml), ipratropium bromide + fenoterol 0.5 ml (10 drops) for children under 6 years of age and 1 ml (20 drops) for children over 6 years of age over 5-10 minutes. Inhalation glucocorticosteroids are used: 0.5-1 mg budesonide in nebules, 1-2 mg/kg prednisolone parenterally. Therapy is assessed after 20 minutes. Unsatisfactory effect - repeat dose of bronchodilator, glucocorticoid. In the absence of a metered-dose aerosol inhaler or nebulizer, aminophylline 4-5 mg/kg is administered intravenously by slow jet stream over 10-15 minutes in isotonic sodium chloride solution. After elimination of a mild or moderate attack, it is necessary to continue treatment with beta ₂ -adrenergic agonists every 4-6 hours for 24-48 hours; in case of a moderate attack, it is possible to switch to prolonged bronchodilators (beta ₂ -adrenergic agonists, methylxanthines) until the clinical and functional parameters are normalized. It is necessary to prescribe or correct basic anti-inflammatory therapy.

Algorithm for the treatment of a severe attack of bronchial asthma

Use beta ₂ -adrenergic agonists every 20 minutes for 1 hour, then every 1-4 hours, or perform long-term nebulization.

Nebulizer use is preferred: salbutamol 2.5 mg or ipratropium bromide + fenoterol 0.5-1 ml, budesonide 0.5-1 mg, systemic glucocorticosteroids - 60-120 mg prednisolone intravenously or 2 mg/kg orally. If the patient cannot create a peak expiratory flow, epinephrine is administered subcutaneously at a dose of 0.01 ml/kg or 1 mg/ml, the maximum dose is 0.3 ml. If there is no inhalation equipment (nebulizer and metered-dose inhaler are not available) or if the effect is insufficient, 2.4% aminophylline is administered intravenously by slow jet stream over 20-30 minutes, then (if necessary) intravenously by drip over 6-8 hours. The effectiveness of the treatment is assessed: if the result is satisfactory (improvement of the condition, increase in peak expiratory flow rate, S _a 0 ₂ ), a nebulizer is used every 4-6 hours for 24-48 hours, systemic glucocorticosteroids 1-2 mg/kg every 6 hours; if unsatisfactory (worsening symptoms, no increase in peak expiratory flow rate, S _a 0 ₂ ) - repeated administration of systemic glucocorticosteroids: 2 mg/kg intravenously, intramuscularly [up to a total of 10 mg/kg x day) or per os for children under one year - 1-2 mg/kg x day), 1-5 years - 20 mg/day, over 5 years - 20-60 mg/day; aminophylline - intravenously continuously or fractionally every 4-5 hours under the control of theophylline concentration in the blood.

After the attack has been eliminated, bronchodilators are prescribed every 4 hours: short-acting beta ₂ -agonists for 3-5 days, with possible transfer to prolonged bronchodilators (beta ₂ -adrenomimetics, methylxanthines); systemic corticosteroids intravenously, intramuscularly or per os for 3-5 days (1-2 mg/kg x day) until bronchial obstruction is relieved. Correction of basic corticosteroid therapy by increasing the dose by 1.5-2 times.

Algorithm for the treatment of asthmatic status

Oxygen therapy with 100% oxygen, monitoring of blood pressure, respiratory rate, heart rate, pulse oximetry are required. Prednisolone 2-5 mg/kg or dexamethasone 0.3-0.5 mg/kg intravenously; epinephrine 0.01 ml/kg subcutaneously or 1 mg/ml (maximum dose up to 0.3 ml). If there is no effect, 2.4% 4-6 mg/kg aminophylline is used intravenously for 20-30 minutes, followed by continuation at a dose of 0.6-0.8 mg (Dkg x h), using isotonic sodium chloride solution and 5% glucose solution (1:1). Increasing hypoxia requires intubation, artificial ventilation, infusion therapy with glucose-salt solutions at a dose of 30-50 ml/kg at a rate of 10-15 drops per minute.

Foreign bodies in the respiratory tract and aspiration syndrome

A foreign body can partially or completely obstruct the airway.

Clinical signs of obstruction:

• ineffective cough;
• inspiratory dyspnea with involvement of accessory muscles; participation of the wings of the nose in breathing;
• wheezing sounds when exhaling;
• stridor;
• cyanosis of the skin and mucous membranes.

Balloting foreign bodies

The majority of all aspirated foreign bodies enter the bronchi, and only 10-15% remain at the level of the larynx or oral cavity and can be removed during examination. A constantly acting negative factor is the time elapsed since aspiration. Balloting foreign bodies are singled out into a separate group due to the great danger to life and the clinical features. Most of such bodies have a smooth surface (watermelon, sunflower, corn, pea seeds). When coughing, laughing, or worrying, they easily move in the tracheobronchial tree, air currents throw them to the glottis, irritating the true vocal cords, which close instantly. At this moment, the sound of a foreign body slapping against the closed cords is heard (even at a distance). Sometimes a balloting body gets stuck in the glottis and causes an attack of suffocation. The insidiousness of balloting bodies is that at the moment of aspiration the patient experiences in most cases a short-term attack of suffocation, then his condition improves for some time. With a prolonged spasm of the vocal cords, a fatal outcome is possible.

Fixed foreign bodies

The condition of patients with foreign bodies fixed in the trachea can be severe. A cough appears suddenly, breathing becomes rapid and difficult, retraction of the compliant areas of the chest appears, and acrocyanosis is pronounced. The child tries to take a position that facilitates breathing. The voice is unchanged. Percussion reveals a box-like sound over the entire surface of the lungs; auscultation reveals equally weakened breathing on both sides. Foreign bodies fixed in the bifurcation area of the trachea pose a great danger. During breathing, they can shift to one side or the other and close the entrance to the main bronchus, causing its complete closure with the development of pulmonary atelectasis. The patient's condition then worsens, dyspnea and cyanosis increase.

Aspiration of vomitus often occurs in children in a coma, during anesthesia, in cases of poisoning or CNS depression caused by other reasons, i.e. in cases where the cough mechanism is impaired. Aspiration of food is observed mainly in children in the first 2-3 months of life. When food enters the respiratory tract, reactive edema of the mucous membrane develops; when acidic gastric juice is aspirated, toxic edema of the respiratory tract (Mendelson's syndrome) joins the local reactive edema. Clinical manifestations are rapidly increasing asphyxia, cyanosis, severe laryngo- and bronchospasm, and a drop in blood pressure.

Despite the clear clinical picture indicating the likelihood of foreign body aspiration, diagnosis can be difficult because with most balloting foreign bodies the physical findings are minimal.

First aid - the fastest possible removal of a foreign body, elimination of spasm of the bronchi and bronchioles. In children under 1 year, it is necessary to deliver 5-8 blows to the back (the child is placed on an adult's arm with his stomach down, head below the body), then turn the child over and deliver several pushes to the chest (at the level of the lower third of the sternum, one finger below the nipples). In children over 1 year, perform the Heimlich maneuver (up to 5 times), being behind the sitting or standing child. If the foreign body is visible, it is removed with a carcinoma, tweezers, Magill forceps; vomit, food debris are removed from the oropharynx with suction. After clearing the airways, 100% oxygen is administered using a mask or breathing bag.

Immediate intervention is not indicated in cases of partial airway obstruction (with normal skin color and cough reflex). Digital examination and blind removal of foreign bodies in children is contraindicated due to the possibility of the foreign body moving deeper, leading to complete obstruction.

During emergency care, the patient is placed in a drainage position with the head of the bed lowered. Tracheal intubation and tracheal and bronchial contents aspiration are performed as quickly as possible to eliminate obstruction. An inflatable cuff on the endotracheal tube protects the airways from repeated ingress of vomit. If effective spontaneous breathing is not observed, artificial ventilation is performed. 50 ml of isotonic sodium chloride solution is injected into the airways through the tube, followed by evacuation by suction. The procedure is repeated several times until the airways are completely clear. If intubation is limited, conicotomy, puncture of the cricothyroid ligament, installation of a large-caliber catheter, or puncture of the trachea with 2-3 large-diameter needles are performed. Oxygen therapy with 100% oxygen.

Hospitalization is mandatory even when removing a foreign body; transportation is always in a sitting position.

Pulmonary edema

Pulmonary edema is a pathological increase in the volume of extravascular fluid in the lungs, developing as a result of increased hydrostatic pressure in the pulmonary vessels, decreased oncotic pressure of blood plasma; increased permeability of the vascular wall, intrathoracic pressure and redistribution of blood from the systemic to the pulmonary circulation.

Types of pulmonary edema:

• cardiogenic;
• non-cardiogenic.

In children, non-cardiogenic pulmonary edema occurs more often, caused by a sharp increase in negative pressure in the chest with unresolved airway obstruction, resumption of spontaneous breathing after it has stopped and prolonged cardiopulmonary resuscitation, aspiration, severe hypoxia (increased capillary permeability), drowning. Cardiogenic edema in children develops with left ventricular failure caused by mitral valve defects, arrhythmias, myocarditis, hyperhydration due to excessive infusion therapy.

Clinical signs: shortness of breath, cough with bloody sputum.

Auscultation reveals moist rales, sometimes gurgling breathing. Tachycardia turns into tachyarrhythmia, cardiac arrhythmia; dyspnea with retraction of the compliant areas of the chest. Examination reveals edema in the legs, dilation of the heart borders.

An important indicator is an increase in central venous pressure (15-18 cm H2O).

Respiratory and metabolic acidosis develops.

Treatment of pulmonary edema begins with elevating the patient (the head of the bed is raised). Furosemide is administered intravenously at a dose of 1-2 mg/kg, if there is no effect, the administration is repeated after 15-20 minutes; prednisolone 5-10 mg/kg. Oxygen therapy is mandatory with 40-60% oxygen passed through 33% alcohol; spontaneous breathing in the positive end-expiratory pressure mode. If the measures taken are ineffective, transfer to mechanical ventilation in the positive end-expiratory pressure mode; children over 2 years old are administered 1% trimeperidine intramuscularly or intravenously (0.1 ml/year of life). Hospitalization in the intensive care unit.

Acute intrapleural tension syndrome

Acute tension in the pleural cavity develops as a result of spontaneous or traumatic tension pneumothorax, incorrect medical manipulations. Spontaneous pneumothorax can occur in an apparently healthy child, with bronchial asthma, pneumonia, cystic fibrosis, bronchiectasis.

Pneumothorax is characterized by sudden, rapidly increasing dyspnea and cyanosis, chest pain, pronounced tachycardia with paradoxical pulse, arterial hypotension, and mediastinal shift to the healthy side. Death occurs within minutes from acute hypoxia and electromechanical dissociation.

Emergency care begins with oxygen therapy with 100% oxygen. The main procedure for tension pneumothorax is a puncture of the pleural cavity in a semi-recumbent position under anesthesia (1-2 ml of 0.5% novocaine) in the second intercostal space along the anterior or middle axillary line along the upper edge of the underlying rib. To remove fluid (blood, pus), a puncture is performed in the fifth intercostal space along the middle axillary line. If the patient is unconscious, anesthesia is not administered. When removing the needle, the skin around the puncture is squeezed with fingers and treated with Cleol.

Treatment measures for valvular pneumothorax - passive drainage according to Bulau.

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