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Asphyxia Neonatorum CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well­ being develop as a result of perinatal asphyxia. Central nervous system ab­ normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas­ sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec­ trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef­ fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in­ molecules brought into the alveoli inadequately com­ Pjury in the newborn. Severe birth asphyxia, evi­ pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte­ and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul­ deprivation has been further enriched by investigators monary capillary blood. Asphyxia can be total or par­ from various disciplines in recent years. However, in tial. Total asphyxia occurs when the ingress of oxygen spite of the many advances, the impact of perinatal and the egress of carbon dioxide is entirely halted. asphyxia on neonatal mortality and morbidity is still Partial asphyxia results when the respiratory gas ex­ evident. change has been reduced, but not totally abolished. Prevention of the problem is, of course, preferable For obvious reasons there is no detailed information to treatment. An understanding of the pathophysiology regarding the various chemical and biophysical of asphyxia is necessary to achieve this goal. changes of fetal or neonatal asphyxia in the human. A useful substitute for the missing human model is the observation by Adamsons and co-workers1 and PATHOPHYSIOLOGY AND NATURAL Dawes2 of the natural history of total asphyxia at birth HISTORY in the rhesus monkey fetus. Shortly after the onset of asphyxia, rapid gasping Perinatal asphyxia describes a clinical entity whereby occurs, accompanied by muscular effort and thrashing the fetus or the newborn infant sustains an impairment movements of the arms and legs. This ceases after a in respiratory gas exchange. Neonatal asphyxia re­ little more than a minute, preceding the onset of pri­ flects acute respiratory failure, that is, a rapid decrease mary apnea, which lasts almost 60 seconds. The in alveolar ventilation. The number of oxygen animal then develops a series of spontaneous deep gasps for 4 to 5 minutes, which gradually become weaker and terminate after approximately 8 minutes of total anoxia. Secondary or terminal apnea begins after Submitted, revised, April 5, 1984. the last gasp, and death occurs if asphyxia is not re­ From the Section of Newborn Services, Department of Pediatrics, Uni­ versed within several minutes. When secondary apnea versity of Michigan Medical Center, Ann Arbor, Michigan. Requests for occurs, spontaneous respiration cannot be induced by reprints should be addressed to Dr. Raul C. Banagale, Neonatal Special Care Unit, Emanuel Hospital, 2801 N. Gantenbein, Portland, OR 97227. any sensory stimuli. The longer the delay in initiating c 1986 Appleton-Century-Crofts THE JOURNAL OF FAMILY PRACTICE, VOL. 22, NO. 6: 539-546, 1986 539 ASPHYXIA NEONATORUM adequate ventilation, the longer it will take to initiate regular respirations. TABLE 1. CAUSES OF PERINATAL ASPHYXIA Assuming the changes in humans are similar to those Failure of the respiratory center in the rhesus monkey, are mechanisms possible for a Prematurity newborn infant to protect himself or herself from such Intrauterine hypoxia an insult? It has been postulated that circulatory ad­ Umbilical cord anomalies and accidents justments occur in the human infant during total as­ Hypovolemia secondary to antepartum hemorrhage phyxia. A study of the effects of hypoxia on the rhesus Maternal conditions (cardiovascular problems, pul­ monary disease, toxemia, other systemic illness) monkey fetus by Behrman et al3 indicates that con­ Obstetrical factors comitant with the decrease in total cardiac output, Uterine and cervical malformation there is a redistribution of the available cardiac output Multiple gestation in an attempt to provide oxygenated blood to the more Abnormal presentation vital organs. Scholander,4 in his study of diving seals, Difficult delivery Respiratory obstructive diseases found that the following reflex circulatory adjustments Airway malformation occur when a seal dives: (1) profound bradycardia, (2) Tumors decrease in oxygen consumption, (3) decrease in body Vocal cord paralysis temperature, (4) accumulation of lactic acid in muscle, Meconium aspiration syndrome Primary disorders (5) maintenance of central blood pressure, and (6) Nervous system continued oxygenation of arterial blood at the expense Respiratory muscle of peripheral blood. When the experimental seals re­ Neuromuscular junction turn to the surface, the pre-dive state resumes, and Infections Group B streptococcus and other bacteria after air breathing starts, the lactic acid is removed Viral from the muscles by the bloodstream and is subse­ quently metabolized by the liver. There is, obviously, a fundamental difference be­ tween the diving mammal and the stressed human in­ fant. In the diving mammals, the circulatory changes as mepivacaine and lidocaine, known to be rapidly are not overwhelmed under the condition of a normal transmitted to the fetus, may produce fetal bradycar­ dive. In the asphyxiated infant, however, the circula­ dia and hypotension. Respiratory obstructive diseases tory changes are in response to life-threatening such as airway malformations, tumors, vocal cord pathologic conditions and the protective mechanisms paralysis, and meconium aspiration syndrome may are quickly exhausted after short periods of asphyxia. also result in neonatal asphyxia. Primary disorders in­ Therefore, assuming there is some circulatory adapta­ volving the nervous system, respiratory muscles, and tion, such as a redistribution of the available cardiac neuromuscular junction (such as neonatal myasthenia output and provision of oxygenated blood to vital or­ gravis) are rare, but are also potential causes. gans such as the brain, heart, and adrenal glands, it Intrauterine pneumonia and sepsis may result in se­ must be at the expense of the kidneys, spleen, lungs, vere perinatal asphyxia. and intestine. As a result, the newborn human is still likely to suffer many possible complications. BIOCHEMICAL CHANGES DURING ASPHYXIA Of the different biochemical events (Table 2) occurring as a result of asphyxia, the most important is the con­ ETIOLOGY version from aerobic oxidation of glucose to anaerobic glycolysis. This conversion leads to accumulation of Table 1 lists the different causes of impairment in res­ lactic acid and the development of metabolic acidosis. piratory gas exchange. Failure of the respiratory center Respiratory acidosis may also occur because of the has been associated with prematurity, intrauterine rapid elevation of PaC02. A profound drop in pH is, hypoxia, obstetrical complications, and administration therefore, the result of a mixed acidosis coincidental of drugs. Prolapse and compression of the umbilical with the hypoxia. Free fatty acids and glycerol, prod­ cord, hypovolemia (resulting from placenta previa, ucts of neutral fat hydrolysis, increase in the blood in abruptio placenta, or any other form of blood loss), response to hypoxia, which may be mobilized by the and umbilical cord or placental anomalies can lead to release of epinephrine and norepinephrine. During intrauterine hypoxia. Other obstetrical problems that labor, maternal blood glucose is elevated secondary to may lead to severe perinatal asphyxia include uterine sympathetic stimulation, leading to a corresponding and cervical malformation, multifetal gestation, ab­ blood sugar elevation in the fetus. When the maternal normal presentation, and traumatic delivery. Adminis­ blood glucose supply is terminated at birth, tration of certain drugs including local anesthetics such glycogenojysis begins immediately to provide a con- 540 THE JOURNAL OF FAMILY PRACTICE, VOL. 22, NO. 6, 1986 asphyxia n eo n a to r u m TABLE 2. BIOCHEMICAL CHANGES RESULTING FROM these conditions in asphyxiated newborns have been ASPHYXIA described extensively.9 The role of asphyxia in the production of central Respiratory and metabolic acidosis nervous system hemorrhage is multifactorial. First, Increased free fatty acids and glycerol hypoxia is associated with impairment of vascular au­ Mobilization of hepatic glycogen toregulation.10 Second, asphyxia produces augmenta­ Hyperkalemia and amino acidemia Hypocalcemia
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