Symptoms.
1. cyanotic or pale skin on the face and body after delivery of the fetus, with dark purple lips and mouth.
2, shallow breathing, irregular or no breathing or only wheezing-like faint breathing.
3, regular heartbeat, with a heart rate of 80-120 beats/minute or irregular heartbeat, with a heart rate of <80 beats/minute and weak.
4.Response to external stimuli, good muscle tone or no response to external stimuli, loose muscle tone.
5. Presence or absence of laryngeal reflex.
Diagnosis based on.
1, bruising of the skin on the face and body of the newborn.
2, shallow or irregular breathing.
3, regular heartbeat, strong and powerful, heart rate 80-120 beats/min.
4, response to external stimuli, good muscle tone.
5.The laryngeal reflex exists.
6, with the above performance is mild asphyxia, Apgar score 4-7 points.
7, pale skin and dark purple lips.
8, no respiration or only wheezing-like faint respiration.
9, Irregular heartbeat. Heart rate <80 beats/min and weak.
10, no response to external stimuli, muscle tone is relaxed.
11.Glottal reflex disappears.
12, with 7-11 items for severe asphyxia, Apgar score 0-3.
Laboratory tests
Blood chemistry tests show respiratory and metabolic acidosis. When asphyxia causes renal impairment, glomerular filtration rate is reduced, renal tubular reabsorption is impaired, and protein, red blood cells and granular tubularity are seen in the first urine discharge, and blood urea nitrogen is increased. Serum and urinary β2-microglobubin (β2-microglobin, β2-MG), concentration increase can be done for those who have the condition. Urinary Nacetyl-β-D-aminoglucosidase (N-acetyl-β-D-glucosaminidase, NAG) lysozyme (Lzm) content increased, urinary amino acid excretion increased. Serum glutathione transaminase GOT, lactate dehydrogenase LDH, phosphocreatine kinase CPK and their isoenzyme measurements are elevated after asphyxia, which helps in the determination of cardiac and cerebral damage.
Differential diagnosis
(a) Neonatal pulmonary hyaline membrane disease.
(b) Neonatal wet lung is most often seen in term cesarean section babies.
There is a history of intrauterine distress, and shortness of breath and cyanosis often appear within 6 hours after birth, but the child is generally well and the symptoms disappear within about 2 days. Moderate to loud wet rales can be heard in both lungs with low breath sounds. Pulmonary X-rays show thickened lung texture, small flaky granular or nodular shadows, interlobular pleural or pleural effusion, and often emphysema as well. However, the lung lesions recover better and often disappear within 3-4 days.
(C) Neonatal aspiration syndrome
(D) Neonatal esophageal atresia Neonatal esophageal atresia is mostly classified by Gross’ five types before.
Type 1: esophageal atresia with two blind ends in the upper and lower segments.
Type 2: The upper part of the esophagus is connected to the trachea and the lower part is the eye-end.
Type 3: The upper segment of the esophagus has a blind end, and the beginning of the lower segment is connected to the trachea.
Type 4: Both upper and lower segments of the esophagus are connected to the trachea.
Type 5: There is no esophageal atresia, but there is a fistula that connects to the trachea. This shows that. Except for type I esophageal atresia. All other types of esophageal atresia have a fistula with the trachea.
When choking, cyanosis and asphyxia occur in newborn infants after oral secretion and feeding, a hard and soft catheter is inserted into the esophagus through the nose or mouth, and if the catheter returns automatically, the disease should be suspected, but a definite diagnosis must be made with iodine oil for esophagogram.
(E) Newborns with postnasal atresia have severe inspiratory difficulties after birth, cyanosis, cyanosis is reduced or disappears when opening the mouth or crying, and respiratory difficulties when closing the mouth and sucking milk, resulting in no weight gain or severe malnutrition due to difficulties in breastfeeding. According to the above manifestations, when the disease is suspected, the tongue can be pressed down with a tongue depressor, and the respiratory difficulty of the child will be relieved. A small amount of gentian violet or melanin can be injected from the anterior nostril to observe whether it can flow to the pharynx, and if necessary, use iodine oil to drop into the nasal cavity for x-ray examination.
(6) Newborn infants with submandibular cleft and cleft palate deformities are born with small jaws, sometimes accompanied by cleft palate, tongue drooping behind the pharynx, resulting in difficulty in inspiration, especially in supine position, head tilted back when breathing, sunken ribs, inspiration with wheezing and paroxysmal bruising, and later with deformity of the qu and wasting. Sometimes the child also has other deformities, such as congenital heart disease, horseshoe foot, syndactyly, cataract or mental retardation.
（On physical examination, the respiratory motion on the left side of the chest is reduced, the percussion is bulbous or turbid on the left side, the breath sounds are low or absent on auscultation, and sometimes intestinal sounds can be heard, and the cardiac turbinates and apical pulsations are shifted to the right side, with a navicular abdomen.
(H) congenital laryngeal webbing after birth with weak cry, hoarseness or loss of voice, inspiration with laryngeal tones and soft tissue invagination in the chest, sometimes inspiration and expiration are difficult, confirming the diagnosis relies on laryngoscopy, which can directly see the laryngeal webbing.
(ix) congenital heart disease, complications of asphyxia when hypoxia, not limited to the heart and lungs, but systemic damage to multiple organs, serious cases are often accompanied by complications.
1, cerebral hypoxia ischemic encephalopathy is the main complication after neonatal asphyxia, due to the involvement of the blood-brain barrier during asphyxia hypoxia, plasma proteins and water extravasation through the blood vessels caused by cerebral edema, swollen cells compress the cerebral vessels, reducing blood flow, resulting in tissue ischemia aggravated by hypoxia, eventually leading to neuronal necrosis of brain tissue. Hypoxia is also often accompanied by hypercapnia, leading to a decrease in pH, disruption of cerebrovascular regulation, and a decrease in arterial blood pressure, causing insufficient blood supply. This causes cerebral white matter infarction, and the white matter around the anterior middle and posterior cerebral arteries farthest from the heart, such as the parsagittal area, can become vascularly infarcted and white matter softened, so HIE is hypoxic. The clinical diagnostic basis and grading criteria (Jinan Conference 1989) for ischemia as a mutually causal lesion are
(1) With a clear history of perinatal hypoxia. In particular, severe perinatal asphyxia.
(2) The following abnormal neurological symptoms appear within 12 hours after birth: disorders of consciousness: such as hyperexcitability (trembling of limbs, prolonged eye opening, staring, etc.), drowsiness, lethargy or even coma, changes in limb tone, such as hypotonia, flaccidity, abnormal primitive reflexes, such as overactive embrace reflex, weakening or disappearance, and weakening or disappearance of sucking reflex.
(3) In severe cases, there may be convulsions, and attention should be paid to the characteristics of neonatal convulsions, such as irregular and irregular rhythmic jerking of the face and limbs, eye gaze, tremor accompanied by apnea, and cyanosis.
(4) In severe cases, central respiratory failure, pupillary changes, intermittent increased extensor tone, and other brainstem injury manifestations are seen.
Changes such as low voltage isoelectricity and burst suppression waveforms seen in EEG are helpful for diagnosis and grading. Narrowing or disappearance of ventricles and generalized echogenicity seen in ultrasound examination within one week after birth suggest cerebral edema. After one week, posterior changes of cerebral edema, such as cerebral atrophy and foramen ovale, are commonly seen. A hyperechoic area behind the lateral ventricular external horn suggests the possibility of periventricular white matter softening. Scattered hyperechoic areas are often due to brain parenchymal ischemia, and restricted hyperechoic areas suggest ischemia in the cerebrovascular distribution of the region, and CT examination is more helpful, as seen in scattered. Focal hypoechoic shadow distribution of 2 lobes is mild, hypoechoic shadow more than 2 lobes gray-white matter contrast blurred is moderate, diffuse hypoechoic shadow gray-white matter boundary loss but the basal ganglia, cerebellum still has normal density, lateral ventricular stenosis compression is severe moderate to severe often accompanied by spider subretina, intracerebroventricular or parenchymal hemorrhage.
2, heart due to hypoxia affects the conduction system and myocardium, atrioventricular conduction is prolonged in mild cases, T-wave flattening or inversion, in severe cases, the heart rhythm is arrhythmic or slow, and systolic murmurs can often be heard. In acidosis, myocardial contraction is weakened and output is reduced, and blood pressure drops, further affecting the perfusion of coronary and cerebral arteries, and finally heart failure occurs. The incidence of heart failure after asphyxia is 22.5%. Echocardiography is an important basis for post-asphyxia heart failure if right-to-left shunt is seen at the atrial level. Doppler measurement of cardiac output can observe the degree of cardiac impairment and its recovery.
Pulmonary manifestation is mainly respiratory disturbance, based on the amniotic fluid aspiration is easy to secondary pneumonia, after active resuscitation still need to pay attention to the pneumothorax, with pulmonary edema and pulmonary vasospasm can be accompanied by ventilation diffusion disorders. Increased pulmonary artery pressure can prompt the arterial duct to reopen to restore fetal circulation, aggravating hypoxia can lead to damage to lung tissue and pulmonary hemorrhage.
4, hepatic asphyxia hypoxia can reduce the linkage between bilirubin and albumin, making jaundice deepen and prolong, also can be prone to DIC due to liver damage and the reduction of coagulation factors such as II Ⅴ Ⅶ Ⅸ and X.
5, other severe asphyxia children with low renal function is prone to hyponatremia, the gastrointestinal tract by the redistribution of blood susceptible to necrotizing small intestine colitis, due to anaerobic metabolism glycogen consumption increased dramatically, prone to hypoglycemia, calcium regulation is weakened, prone to hypocalcemia.