Asphyxia etymologically means breathlessness or shortness of breath.

Clinically, it is a syndrome characterized by severe suspension decreased gas exchange at the level of the placenta or lungs, resulting in hypoxemia, hypercapnia and tissue hypoxia with metabolic acidosis. Asphyxia is often accompanied by ischemia, which in turn aggravates tissue hypoxia, and accumulation of products of cell catabolism. Perinatal asphyxia speak because it can occur before birth, during pregnancy, labor and delivery, as well as after birth. Choking affects all organ systems to varying degrees depending on its intensity and duration. It is in the central nervous system where the injury occurs most relevant for their consequences in terms of mortality and sequelae. The damage caused by suffocation last term will depend on the extent to which altered oxygen delivery to the tissues, which depends on: the amount of oxygen in arterial blood, which is determined by the concentration of hemoglobin and hemoglobin type Pa02 and adequate circulation The incidence of asphyxia varies in different centers and diagnostic definition is given. Can be estimated at about 0.2 to 0.4% of newborns. Etiology The vast majority of cases are of perinatal hypoxic intrauterine origin. Approximately 5% occur before the onset of labor, 85% during labor and second stage and 10% during the neonatal period. (Volpe). Intrauterine Asphyxia at birth is expressed clinically as cardiorespiratory depression, if not treated early aggravate this condition. Other causes that may occur as cardiorespiratory depression are: congenital malformations, prematurity, neuromuscular and CNS depressant drugs administered to the mother during labor. Obstetric causes most frequently associated with perinatal asphyxia are: Factors antepartum intrapartum factors Hypertension with toxemia of pregnancy Presentation dystocia Anemia or iso-immunization Decreased fetal activity acute bleeding Abnormal fetal heart rate maternal infection Meconium in amniotic fluid

diabetes hypertonic uterine Premature Rupture of Membranes Cord prolapse Post-term pregnancy Circulars irreducible Asphyxia occurs mainly alterations in respiratory and circulatory physiology. These are similar in the fetus and newborn. As a result of these decreases the oxygen supply to tissues and disrupts the metabolism and cell function. The fetus and newborn have a better capacity to adapt to situations of hypoxia, due to its lower energy use and increased tissue glycogen content of the heart muscle, allowing them to maintain cardiac function for more prolonged periods than the adult.

Hypoxia results in a sequence of events: Initial period of deep breathing (gasping) Cessation of breathing movements: primary apnea, cyanosis but no muscle tone is preserved. At this time can restart breathing in most cases with tactile and O2 delivery. If choking continues to occur: Period gasping deep breaths Secondary apnea manifested as cyanosis and pallor, hypotension and absence of tone and reflexes. In this period in RN responds to stimuli and can die if not promptly initiated ventilation with oxygen. There are decreased cardiac output and redistribution of privileging the flow to brain, heart, adrenal and placenta (fetus) to the detriment of the flow to the lungs, kidneys, intestine and skeletal muscle ("Diving reflex".) Pulmonary vascular resistance and pressure increase the pulmonary artery in the newborn maintaining a circulation pattern more difficult fetal oxygenation in ventilated child. CLINICAL AND DIAGNOSTIC

Fetal asphyxia multisystem involvement occurs, therefore, the symptoms depend on the extent to which each organ has been affected. In some cases there is only a single organ manifestations. The most affected are the kidney, CNS, cardiovascular and lung. Central Nervous System. Is the body more vulnerable because of poor regeneration capacity and the possible consequences that may be. The most characteristic clinical manifestations have been encompassed under the term hypoxic-ischemic encephalopathy. Determining the degree of encephalopathy allows therapeutic and prognostic orientation of asphyxiation, so are described in Table 9.1 In the early RN these manifestations are not so clear so this classification is not applicable in this group is committed globally RN muscle tone and brain stem functions. The encephalopathy grade I, are a good prognosis, degree II is associated with a 20 to 30% of longterm neurological sequelae and serious commitment, grade III, has a 50% mortality in the neonatal period and those who survive, over 95% of them left with severe sequelae. Cardiovascular System A cause asphyxia cardiac level transient myocardial ischemia. You have signs of heart failure with tachypnea, cyanosis, tachycardia, gallop rhythm and hepatomegaly in varying degrees. It is more common than either right ventricular failure, which may involve the papillary muscle with tricuspid regurgitation manifested in a breath auscultable on the left edge of the sternum. No increase from 5 to 10 times, the cardiac isoenzyme of creatine phosphokinase. Early diagnosis and treatment of this complication determines the immediate newborn survival suffocated. Respiratory System. The most common box is Meconium Aspiration Syndrome often associated with varying degrees of Persistent Pulmonary Hypertension Kidney and urinary tract. Decreased renal perfusion secondary to cardiac deldbito redistribution and hypoxemia explain observaen renal involvement is a large percentage of asphyxiated newborns. Lesions observanson tubular necrosis and myoglobin deposit derived from tissue destruction. Syndrome can occur inapropiadade antidiuretic hormone secretion. Clinically detected oliguria, nitrogen retention and hypertension. The sluggishness of the urinary tract can lead to bladder paralysis. Choking is probably the most common cause of acute renal failure in the neonatal period. Digestive System. Decreased intestinal transit, stress ulcers and intestinal necrosis have been described in infants suffocated, however this relationship is not constant. Intestinal ischemia is one of the factors predisposing to necrotizing enterocolitis.

Hematologic and liver. Leukopenia, leukocytosis with left shift and thrombocytopenia may be observed as a result of hypoxia and spinal stress. In severe asphyxia capillary endothelial damage occurs clotting productsfrom consumption which is aggravated by decreased hepatic, this leads to disseminated intravascular coagulation. It is frequently elevated transaminases (SGOT, SGPT), GGT and blood ammonia. Prothrombin can be decreased. Metabolic Commitment. The metabolic acidosis is the most typical dehipoxia and / or tissue ischemia, at the time of birth can diagnose acidosis by measuring pH in a sample of umbilical artery. RN consider the acidotic blood whose pH is less than 7.11, is considered a serious acidosis a pH below 7.0, the large consumption of glucose characteristic of anaerobic glycolysis, and increased calcitonin secretion observed in RN explained hypoglycemia asphyxiated and hypocalcemia may occur in the first 24-48 hours of life. The clinical diagnosis of asphyxia has been the subject of many different definitions. Traditionally used Apgar score. However, it has limitations since it can be low in preterm infants without asphyxia and maternal drug depressed children. The Apgar 1 also has little predictive value in neurological sequelae. In the Neonatal Unit of the Catholic University, we have expanded this approach, we consider those RN suffocated submit at least two of the following records: Fetal distress Fetal acidosis (umbilical artery pH <7.11) Apgar = <3 per minute and / or = <6 at 5 minutes Clinical Manifestations asphyxia (hypoxic-ischemic encephalopathy, meconium aspiration, persistent pulmonary hypertension, acute renal failure, cardiogenic shock). Prevention and Treatment. Prevention includes all measures of good prenatal care and delivery care. The perinatal possible to identify the majority of children born with asphyxia and cardiorespiratory depression, so be prepared for a good revival and eventual transfer of the child to an intensive care unit. In managing resuscitation following asphyxia is useful to classify in three categories according to the degree of clinical compromise: Slight under the following conditions: Acute fetal distress. Apgar <3 at one minute and> 7 at 5 minutes. umbilical artery pH> 7.11

Absence of symptoms. The behavior in these cases is checking vital signs for 4-6 hrs and if it stays asymptomatic shipped with your with your mother. Moderate A previous conditions is added: * 3 to 5 Apgar at 5 minutes and / or umbilical artery pH <7.11 (in the absence of symptoms). In these cases the children should be observed for at least 12-24 hours. If sensory engagement should be hospitalized. Feeding should be delayed until it stabilizes the cardiovascular reflex is restored ausculten suction and bowel sounds. Serious Is considered severe when the Apgar score at 5 minutes is <3, the pH <7.0 and / or clinical manifestations appear asphyxia (meconium aspiration hypoxic ischemic encephalopathy, etc..) These children require always be treated promptly in Intensive Care Unit because they require continuous monitoring of vital signs and specific treatments according to the organs affected. Some of them have seizures and require early early be given an initial dose of 20mg/kg phenobarbital ev slow. Supplementary examinations: Brain ultrasonography, the first, within 72 hours of life and then weekly until 3 weeks. TAC. at 72 h and 3rd week of life. EEG And early neurological examination at discharge. Brain and cardiac isoenzymes. Coagulation tests, electrolytes, serum calcium, urea nitrogen, arterial blood gases CBC. Treatment: General: Keep cardiorespiratory function in normal range by O2 and / or mechanical ventilation. Keeping blood pressure using vasoactive drugs to support cerebral perfusion. Correct metabolic acidosis and hypoglycemia.

Correct hypovolemia and / or anemia. Use of anticonvulsants. Specific (are experimental therapies) General and targeted Hypothermia Skull Free radicals Removers (Allopurinol) Calcium blockers. Excitatory amino acid antagonists (glutamine) Prognosis The prognosis of perinatal asphyxia is difficult to pinpoint. Only long-term monitoring ensures normal psychomotor. Poor prognostic factors are: Hypoxic Encephalopathy Grade II and III of Sarnat. Early and prolonged convulsions. Cardiorespiratory failure. Cerebral abnormal EEG and ECO. Abnormal neurological examination at discharge. The aftermath more features are cerebral palsy, seizures, psychomotor retardation and perceptual deficits