Asphyxia

Introduction Asphyxia: As the body's respiratory process is blocked or abnormal for some reason, the resulting pathological state of tissue and cell metabolism, dysfunction and morphological damage caused by carbon dioxide retention is called asphyxia. When the body is severely deprived of oxygen, organs and tissues are extensively damaged and necrotic due to lack of oxygen, especially the brain. The airway is completely blocked and can't be breathed for only 1 minute, and the heartbeat will stop. As long as the rescue is timely, the airway is blocked, the breathing is restored, and the heartbeat is restored. However, asphyxia is one of the most important causes of death in critical illness.

Cause

1, mechanical asphyxia, due to mechanical effects caused by respiratory disorders, such as sputum, twisting, neck, the use of obstructed breathing channels, compression of the chest and abdomen and suffering from acute laryngeal edema or food intake tracheal caused by asphyxia.

2, toxic asphyxiation, such as carbon monoxide poisoning, a large amount of carbon monoxide from the respiratory tract into the lungs, into the blood, combined with hemoglobin into carboxyhemoglobin, hindering the combination and dissociation of oxygen and hemoglobin, leading to suffocation caused by tissue hypoxia.

3, pathological asphyxia, such as water and pneumonia caused by the loss of respiratory area; 4 central circulatory dysfunction caused by cerebral circulation disorders; 5 neonatal asphyxia and air anoxic suffocation (such as closed into the box, cabinet, air The oxygen in the gradual decrease, etc.). Symptoms are mainly characterized by the stimulation of symptoms caused by the accumulation of carbon dioxide or other acidic metabolites and the symptoms of central nervous paralysis caused by hypoxia.

an examination

Related inspection

Carotid pulsation pulse

1. The face and body skin are bruising.

2. Breathing is superficial or irregular.

3. Heartbeat rules, strong and powerful, heart rate 80-120 beats / min.

4. Respond to external stimuli and have good muscle tone.

5. Laryngeal reflex exists.

6. With the above performance as mild asphyxia, Apgar scored 4-7 points.

7. The skin is pale and the lips are dark purple.

8. No breathing or only breathing like a weak breath.

9. The heartbeat is irregular, the heart rate is <80 beats/min, and weak.

10. No response to external stimuli, muscle tension is relaxed.

11. Throat reflex disappears.

12. With 7-11 items for severe asphyxia, Apgar scores 0-3 points.

Differential diagnosis

(1) Neonatal hyaline membrane disease

Also known as neonatal respiratory distress syndrome, it is pointed out that soon after birth, progressive dyspnea, bruising, expiratory sputum, inspiratory tri-concavity and respiratory failure are mainly seen in premature infants.

(two) neonatal wet lung

More common in full-term cesarean section, there is a history of intrauterine distress, often within 6 hours after birth, shortness of breath and cyanosis, but the general condition of the child is good, the symptoms disappear within about 2 days. Both lungs can smell medium and large wet rales, low breath sounds, lung X-rays show thickening of lung texture, small pieces of granules or nodular shadows, effusion in the pleural or thoracic cavity between the leaves. There is also emphysema, but the lung lesions recover better, often disappear within 3 to 4 days.

(3) Neonatal inhalation syndrome

An important part of the differential diagnosis of neonatal asphyxia.

(4) Neonatal esophageal atresia

Newborn esophageal atresia is more commonly used in the classification of Gross five types:

Type 1: The upper and lower segments of the esophageal atresia are two blind ends.

Type 2: The upper end of the esophagus is connected to the trachea and the lower end is the end.

Type 3: The upper part of the esophagus is a blind end, and the initial part of the lower part is connected to the trachea.

Type 4: Both the upper and lower esophagus are connected to the trachea.

Type 5: no esophageal atresia, but there is a fistula connected to the trachea. It can be seen that except for the type I, the esophageal atresia has traffic congestion in all other types of esophagus and trachea.

When the newborn baby's oral secretions increase, when coughing, purpura and asphyxia appear after feeding, use a soft and moderate catheter, insert the esophagus through the nose or mouth. If the catheter returns automatically, the disease should be suspected, but the diagnosis must be made. Iodine oil was used for esophagography.

(5) Neonatal nasal posterior atresia

After birth, there is a serious difficulty in inhaling, cyanosis, and when the mouth is open or crying, the hair loss is reduced or disappeared. There are breathing difficulties when closing and sucking. Poor weight or severe malnutrition due to difficulty in feeding the patient. According to the above performance, when the disease is suspected, the tongue can be pressed down with a tongue depressor, and the child is relieved of breathing difficulties. Or in the case of maintaining the mouth of the child, use a thin catheter to insert from the anterior nares to see if you can enter the pharynx or use a stethoscope to align the left and right nostrils of the newborn, and listen to air rushing out. You can also use cotton silk in the nose. Observe whether the swing is to determine whether the nostrils are ventilated. A small amount of gentian violet or Meilan can also be injected from the front nostril to see if it can flow to the pharynx. If necessary, use iodized oil to drip into the nasal cavity and perform X-ray examination.

(6) Neonatal submandibular and cleft palate

When the baby is born, the jaw is small, sometimes accompanied by a split, and the tongue is drooping to the back of the throat, making it difficult to inhale. Especially in the supine position, breathing difficulties are significant. When breathing, the head leans back, the ribs are sunken, and the inhalation is accompanied by wheezing and paroxysmal bruising. Later, chest deformities and weight loss occur. Sometimes the child is accompanied by other deformities. Such as congenital heart disease, clubfoot, finger (toe), cataract or mental retardation.

(7) Newborns

Difficulty breathing and persistent and paroxysmal purpura after birth, accompanied by intractable vomiting. During the physical examination, the respiratory movement on the left side of the chest was weakened, and the left side of the percussion was drum sound or dull sound, and the auscultation breath sound was low or disappeared. Sometimes bowel sounds can be heard. The heart sounds and the apex beats to the right. A scaphoid, X-ray chest and abdomen perspective or photo can be diagnosed.

(8) Congenital throat

After birth, the crying is weak, and the voice is hoarse or silent. Inhalation is accompanied by throat and chest soft tissue invagination. Sometimes it is difficult to inhale and exhale. The diagnosis depends on the laryngoscopy and can be seen directly in the throat.

(9) Congenital heart disease.

(10) Group B hemolytic streptococcus (GBS) pneumonia

It can be seen in premature, near-term and full-term neonates. The mother has a history of infection and premature rupture of amniotic membrane in the late pregnancy. The clinical characteristics of the disease are the same as those of premature infants. Chest X-ray examination showed signs of inflammation of the lobe or segment and alveolar collapse. The clinical signs of infection were 1 to 2 weeks. The treatment is performed with a combination of broad-spectrum antibiotics such as ampicillin plus gentamicin for the first 3 days after birth, followed by 7-10 days of ampicillin or penicillin. The dose requirement is to refer to the minimum inhibitory concentration to avoid loss due to low dose.

(11) Hereditary SP-B deficiency

Also known as "congenital pulmonary surfactant protein deficiency", it was discovered in the United States in 1993, and there are currently more than 100 children diagnosed with molecular biology techniques in the world. The cause of the disease is a mutation in the DNA sequence that regulates SP-B synthesis. Clinically, children born in full-term have progressive dyspnea and are ineffective by any treatment intervention. There may be a family morbidity. The pathological manifestations of lungs were similar to those of premature infants. The lung biopsy found that SP-B protein and SP-B mRNA were absent, and could be associated with abnormalities in the synthesis and expression of pre-SP-C. The lung tissue pathology was similar to alveolar proteinosis. Exogenous pulmonary surfactant treatment can only temporarily relieve symptoms, and children rely on lung transplantation, otherwise they will die within 1 year of age.

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