Atelectasis of the newborn

Introduction

Introduction to neonatal atelectasis Strictly speaking, atelectasis should indicate that the lungs have never filled the gas after birth, and the de-aeration of the already inflated lung tissue should be called pulmonary collapse. However, due to years of habits, generalized atelectasis can include congenital atelectasis and acquired lung collapse. basic knowledge The proportion of illness: 0.001% Susceptible population: newborn Mode of infection: non-infectious Complications: bronchiectasis, lung abscess

Cause

Neonatal atelectasis

The lung parenchyma or bronchus is compressed (35%):

(1) Thoracic dyskinesia: abnormalities in nerves, muscles and bones, such as cerebral palsy, polio, polyneuritis, spinal muscular atrophy, myasthenia gravis and skeletal deformities (rickets, funnel chest, scoliosis) Wait.

(2) diaphragmatic dyskinesia: due to paralysis of the phrenic nerve or increased intra-abdominal pressure, often caused by a large number of ascites caused by various reasons.

(3) lung expansion is limited: due to negative pressure or increased pressure in the thoracic cavity, such as pleural effusion, gas accumulation, empyema, hemothorax, chylothorax, tension pneumothorax, sputum, tumor and heart enlargement.

(4) bronchial compression by external force: due to enlarged lymph nodes, tumor or cyst compression, bronchial lumen blockage, air can not enter the lung tissue, enlarged left atrium and pulmonary artery can compress left common bronchus leading to left atelectasis.

Obstruction in the bronchi or bronchioles (25%):

(1) foreign body: foreign body block bronchus or bronchioles cause lobary or segmental atelectasis, occasional foreign body block the trachea or main bronchus caused by bilateral or one side of atelectasis.

(2) bronchial lesions: bronchial submucosal tuberculosis, tuberculosis granulation tissue, diphtheria pseudomembrane and trachea and bronchus.

(3) bronchial wall sputum and viscous secretions in the lumen: the baby's respiratory tract is narrow, easy to be blocked, suffering from pulmonary inflammatory diseases such as pneumonia, bronchitis, whooping cough, measles, etc., and bronchial asthma, bronchial mucosa Swelling, smooth muscle spasm, viscous secretions can block the airway and cause atelectasis. These causes are more common in winter and spring. Therefore, the incidence of atelectasis is also more in the cold season. Cough medicines such as opioids and atropine can reduce the natural Coughing, which can make the secretions thicker, can increase obstruction, so it can not be abused.

When poliomyelitis or other causes of diaphragmatic muscles and chest muscles are low or even paralyzed, bronchial secretions are not easy to cough up, in the case of chest surgery for a long period of general anesthesia, deep anesthesia or traumatic shock, bronchial due to stimulation Hey, the bronchial secretions have been increased, such as cough reflexes are inhibited or disappeared, secretions are more likely to block the lumen, causing atelectasis.

Bronchiolitis, interstitial pneumonia and bronchial asthma often cause obstruction of most bronchioles. The initial manifestation is obstructive emphysema, followed by partial obstruction, which forms atelectasis and coexist with emphysema.

According to the results of direct examination by bronchoscopy, the formation of obstructive atelectasis can be elucidated.

Non-obstructive atelectasis (25%):

(1) Surfactant deficiency: Pulmonary surfactant is produced by type II alveolar epithelial cells and is a phospholipid protein complex. The main function is di-brownoyl lecithin, and the surfactant is coated on the alveoli. The inner surface has the function of lowering the surface tension of the air-liquid interface of the alveoli, and has the function of stabilizing the alveolar to prevent alveolar collapse. If the surface active substance is lacking, the surface tension of the alveoli is increased, the alveolar retractive force is increased, and the alveoli is collapsed, resulting in Many places with micro atlasement (microatelectasis), pulmonary surfactant deficiency can be seen in:

1 The lungs of premature infants are immature.

2 Bronchial pneumonia, especially viral pneumonia, reduces the production of surfactants.

3 Injury, shock and other initial hyperventilation, rapid consumption of surface active substances.

4 Inhalation of toxic gas or pulmonary edema may destroy and denature the surfactant. The surface tension of normal lung is 6 dynes/cm. When the surfactant is deficient, the surface tension of infants with respiratory distress may reach 23 dynes/cm.

(2) Another type of non-obstructive atelectasis may be related to the neuromuscular structure of the terminal airway of the lung: Many scholars have confirmed that there is a muscle elastic fiber in the alveolar duct and alveolar sac, which is interwoven with smooth muscle and elastic fibers. Together, controlled by autonomic nerves, when severe pain such as rib fractures and surgery, or when the bronchi is strongly stimulated, such as bronchography, contraction of muscle elastic fibers can cause atelectasis, especially large lung collapse.

(3) too shallow breathing: such as after surgery and application of morphine, or coma and extremely debilitated patients can see superficial breathing, when the pressure in the lungs is reduced enough to resist local surface tension, it can gradually cause alveolar closure and lung Zhang, encourage deep breathing of the patient after surgery to prevent the alveoli from closing, or to reopen the alveoli that is closed due to shallow breathing.

In short, the incidence of atelectasis in children is higher, the cause is bronchiolitis, bronchitis, asthma, bronchial lymph node tuberculosis, multiple radiculitis, bronchial foreign body and more after surgery, in addition, can also be seen in inhalation Pneumonia, bronchiectasis, intracranial hemorrhage, endocardial fibroelastosis, congenital heart disease, tumors, etc.

Prevention

Neonatal atelectasis prevention

Specific preventive measures: use a tracheal tube that is slightly thinner than a sealed airbag; intratracheal irrigation and intra-tracheal temperature and humidification; strengthen chest physical therapy; mechanical ventilation plus PEEP to prevent end-expiratory alveolar collapse; , before and after extubation (intravenous bolus dexamethasone, sucking, atomizing, flapping back, turning over).

Complication

Neonatal atelectasis complications Complications, bronchiectasis, lung abscess

If the atelectasis persists for a long time, it is easy to have secondary infection on the basis of atelectasis, causing bronchial damage and inflammatory secretion retention. Bronchiectasis and lung abscess may occur over time.

Symptom

Neonatal atelectasis symptoms common symptoms high fever dyspnea hairy hypoxemia chest pain heart palpitations

1. Symptoms and signs: Because the etiology and scope are different, the symptoms are different. The different degrees of atelectasis are described below.

(1) one or both of the atelectasis: often caused by a variety of reasons, such as pectoral muscle, diaphragmatic paralysis, cough reflex disappearance and bronchial endocrine obstruction, one or both sides of the atelectasis, the onset is very urgent Breathing is extremely difficult. Older children can complain of chest pain and palpitations. They can have high fever, pulse rate and cyanosis. They occur in the latter part of the operation. Most of them occur within 24 hours after surgery. The obvious chest signs are as follows:

1 The ipsilateral thorax is flat and the breathing movement is limited.

2 trachea and apex beat to the disease side.

3 There is a slight dullness at the time of percussion, but it can be covered by the rising stomach on the left side.

4 breath sounds weak or disappear, 5 diaphragm muscles move high.

(2) lobary atelectasis: slow onset, less difficult to breathe, signs similar to total atelectasis, but to a lesser extent, can vary with the lobe of the lobe, upper lobe atelectasis When the trachea moves to the diseased side and the heart does not shift, the percussive dullness is limited to the front chest; when the inferior lobe is inferior, the trachea does not shift and the heart moves to the diseased side, and the percussive dullness is located at the back of the spine; Signs are less, difficult to detect, due to compensatory emphysema in the adjacent area, percussion dullness is often not obvious.

(3) Lung incarceration: clinical symptoms are rare, not easy to detect, atelectasis can occur in any lobe or lung segment, but the left upper lobe is the rarest, only the left lung artery in the congenital heart disease is compressed by the left upper lobe. Causes left at first lobe atelectasis, pediatric atelectasis is most common in the lower lung and right middle lobe; lower atresia infection is more common in the lower left and right middle lobe; tuberculous enlarged lymph nodes cause upper right and middle right lobe Zhang, "middle lobesyndrome" refers to the atelectasis caused by tuberculosis, inflammation, asthma or tumor, does not disappear for a long time, repeated infection, and finally develops into bronchiectasis.

2, pulmonary function test: visible lung capacity reduction, lung compliance decreased, abnormal ventilation / blood flow ratio and degree of arteriovenous shunt, hypoxemia.

3, X-ray examination: X-ray features uniform and dense shadow, occupying one side of the chest, one leaf or lung segment, the shadow has no structure, the lung texture disappears and the volume of the lung leaves shrinks, and the intercostal space narrows when one or a large piece of the atelectasis The thoracic cavity is reduced, and the position of the shadow varies with the location of the atelectasis of each lobe. The atelectasis of the lower lobe is triangularly shadowed in the frontal chest radiograph, located between the spine and the diaphragm, and close to the posterior chest wall in the lateral patch. The leaves are atelectasis, and the front and side shadows are wedge-shaped. The tip is downward and points to the hilum. If the left middle lobe is atelect, the front shadow is triangular, the bottom is at the right edge of the heart, and the tip points to the outside. The silhouette is a wedge shape, the bottom is near the front chest wall, above the diaphragm, the tip is backward and upward, and in the infant period, in addition to compensatory emphysema, other compensatory phenomena such as tracheal and cardiac displacement and diaphragmatic rise It can not appear until the atelectasis lasts for a long time, but due to the lack of surface active substances, the lungs are mostly with a glassy shadow, and the X-ray findings are no different from those of lobular pneumonia.

4, the course of disease: obstructive atelectasis can be short-lived or persistent, pneumonia, bronchiolitis, asthma and bronchitis caused by mucin embolism or mucosal edema, atelectasis, shorter time, easy to disappear after anti-inflammatory swelling, Due to tuberculosis or unextracted foreign body, atelectasis can be more persistent, bilateral or large areas of atelectasis often die quickly, should immediately use a bronchoscope to aspirate the blockage, and artificial resuscitation can survive.

Examine

Neonatal atelectasis

Radiological examination

Radiological examination is the most important means of diagnosing atelectasis. Conventional chest radiographs usually define the presence and location of the leaf or segmental atelectasis. The radiological manifestations of atelectasis vary widely and are often atypical. In the anterior or posterior position of the lack of projection conditions, due to the cover of the heart, the left lower lobe is often missed. Inferior lobe can be mistaken for mediastinal widening, and the effusion is similar to atelectasis, and a large amount of pleural effusion can cover the inferior lobe. Bronchial air sign can rule out complete bronchial obstruction, but can not eliminate lung lobe collapse.

2. Laboratory examination

The routine examination of blood has limited value in the differential diagnosis of atelectasis. Asthma and Pulmonary Aspergillosis with mucus impaction are infected with blood eosinophilia, occasionally in Hodgkin's disease, non-Hodgkin's lymphoma, bronchial lung cancer, and sarcoidosis. Blocking distal secondary infections has neutrophils and increased erythrocyte sedimentation rate. Chronic infections and lymphomas are mostly anemia. Sarcoidosis, amyloidosis, chronic infection, and lymphoma showed increased gamma globulin.

Serological tests for anti-Aspergillus antibodies have a high sensitivity and specificity for the diagnosis of pulmonary allergic Aspergillus infection. The specific complement fixation test can be positive when histoplasmosis and coccidioidomycosis cause bronchoconstriction. The detection of serotonin in blood and urine has diagnostic value for carcinoid syndrome caused by bronchial lung cancer.

3. sputum and bronchial aspirate examination

Because the coughed secretions are mainly from the lungs that do not occur, and can not reflect the pathological process that causes bronchial obstruction, the sputum examination has little diagnostic significance for atelectasis. Smear examination and culture of bacteria, fungi and Mycobacterium tuberculosis should be performed, and cytological examination should be routinely performed. Allergic Aspergillus infection can sometimes produce Aspergillus, but it is necessary to pay attention to the contamination of Aspergillus in the laboratory. If you cough up the sputum and find a large number of hyphae under the microscope, you can establish a diagnosis.

4. Skin test

Skin tests have little effect on the diagnosis of atelectasis. The tuberculin, coccidiostat or histoplasmin skin test can be positive for atelectasis caused by bronchial stones and provide clues for diagnosis. If the atelectasis is caused by the enlargement of the hilar lymphadenopathy, the tuberculin skin test turns positive in the near future, especially in children or adolescents, and has certain diagnostic value. Skin tests in allergic Aspergillus infections are typically immediate skin reactions, and some patients exhibit biphasic responses.

5. Bronchoscopy

Bronchoscopy is one of the most valuable diagnostic tools for atelectasis and can be used in most cases. In most cases, obstructive lesions can be seen directly under the microscope and biopsies taken. If a rigid bronchoscope is used, the stenosis can be dilated and exogenous or endogenous stones removed. If foreign bodies or bronchial stones are surrounded by granulation tissue, it is not easy to confirm the diagnosis under the microscope.

6. Lymph node biopsy and extrathoracic biopsy

If atelectasis is caused by bronchial lung cancer or lymphoma, subscleral muscle and mediastinal lymph node biopsy are helpful for diagnosis, while fiberoptic biopsy is often negative. If there is a clear hilar or mediastinal growth, lymph node biopsy often has a positive finding, and if the radiological changes only the distal lung tissue collapses, it is difficult to obtain a positive result. When sarcoidosis, tuberculosis, and fungal infections cause atelectasis, there are occasional positive findings in the subcutaneous and mediastinal lymph node biopsy. Extrathoracic biopsies (liver, bone, bone marrow, peripheral lymph nodes) can sometimes provide diagnostic assistance for certain diseases such as sarcoidosis, infectious granuloma, lymphoma, and metastatic bronchogenic lung cancer.

7. Pleural effusion examination and pleural biopsy

There are several reasons for the formation of pleural effusion during atelectasis. Pleural effusion may mask the radiological signs of atelectasis. Pleural effusion and pleural biopsy have diagnostic value for malignant lesions and certain inflammatory lesions. The blood chest is seen in a chest trauma or an aneurysm rupture, while a bloody pleural effusion suggests a tumor, pulmonary embolism, tuberculosis or trauma.

Diagnosis

Diagnosis of neonatal atelectasis

diagnosis

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

The disease should be differentiated from neonatal hyaline membrane disease, wet lung, pneumonia, pleural effusion, pulmonary embolism, neonatal asphyxia.

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