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| Question | Answer |
| Intrauterine asphyxia | Either prior to or during delivery there is a reduction in placental gas exchange leading to hypoxia, hypoxemia, and acidosis. This places the infant at a greater risk for perinatal asphyxia |
| Asphyxia | An impairment of gas exchange resulting in severe hypoxia leading to hypoxemia, hypercapnea and mixed acidemia. In the fetus and neonate the two most common categories of asphyxia are intrauterine asphyxia and perinatal asphyxia |
| Perinatal asphyxia | Failure of the newborn to adequately establish respirations leading to an impairment of gas exchange resulting again in hypoxia, hypoxemia, and acidosis |
| Hypoxia | A decreased or inadequate tension of cellular oxygen |
| Hypoxemia | Decreased tension of oxygen in the arterial blood. |
| Ischemia | A decreased blood supply or perfusion to a body part(s) or organ(s) |
| 4 criteria for asphyxia | 1.Umbilical cord blood sample (arterial) with a pH<7.00 2. Apgar score of 0-3 at greater than 5 minutes 3. Clinical neurologic sequelae in the immediate neonatal period such as seizures, hypotonia, coma, or hypoxic-ischemic encephalopathy 4.Evidence of multisystem organ dysfunction |
| Prenatal/Maternal Risk Factors for Asphyxia | preeclampsia hypertension diabetes blood group alloimmunization heart disease drug or alcohol abuse prolonged rupture of membranes maternal infection abruptio placentae placenta previa other antepartum hemorrhage. |
| Fetal Risk Factors for Asphyxia | prematurity postmaturity polyhydramnios oligohydramnios decreased rate of growth fetal malformations low biophysical profile meconium stained amniotic fluid multiple births. |
| Intrapartum Risk Factors for Asphyxia | Breech or other abnormal presentation forceps (other than low elective) vacuum extraction prolapsed cord cord compression prolonged or precipitous labor abnormal heart rate or rhythm |
| Mechanisms of Asphyxia | *altered placental gas exchange *altered maternal perfusion of the placenta *maternal hypoxemia *interruption of umbilical circulation *a compromised fetus *failure of the newborn to establish adequate respirations and adequately transition at birth. |
| ultimate death of the cell is from a combination of all of these effects | Energy failure occurs at the cellular level Acidosis is created Glutamate and nitric oxide are released or created and cause neurotoxicity there is free radical formation Ca++ accumulation (which stimulates a series of destructive events) Lipid perioxidation |
| Fetal Response to Hypoxia/Ischemia: Early | At less than 2 minutes An asphyxial event occurs, the fetus responds with a period of rapid gasping and an increased heart rate. The blood pressure slowly rises. |
| Fetal Response to Hypoxia/Ischemia: Intermediate | The fetus now enters a period of primary apnea where respirations have ceased. The heart rate decreases and there is a gradual decrease in blood pressure. Spontaneous respiration can be induced at this time with tactile stimulation. |
| Fetal Response to Hypoxia/Ischemia: Late | If the event continues (now beyond 2-4 minutes), a second period of deep gasping begins. They increase and then begin to slow down. Heart rate and blood pressure decrease. If the event continues for another 7-8 minutes, respiratory efforts will cease (secondary apnea). There is pronounced bradycardia, lactic acidosis, and cerebral ischemia at this point |
| Fetal Response to Hypoxia/Ischemia: Physiologic adaptation | It is important to remember that the body attempts to adapt to the hypoxic state by preserving cardiac function. The body produces selective vasoconstriction to reduce blood flow to organs less vital than the brain and heart. This increases blood flow to the brain and heart and cardiac output is maintained early in asphyxia. The other organs are, therefore, affected earlier in the asphyxial event than the brain and heart. |
| Clinical Presentation/Recognition of Asphyxiated Infant | A. Abnormal Antepartum/Intrapartum Assessment 1. Know the risk factors and anticipate potential problems before the neonate delivers 2. Get a complete history of pregnancy prior to delivery, if possible 3. Communicate with obstetric team in preparing for infants at risk B. Low Apgar score: especially a low score at 5 minutes C. Low cord pH (less than 7.00) D. Respiratory depression E. Myocardial depression: infant may present with bradycardia, hypotension, and even shock. F. Neurologic symptoms: could range from hyper alertness, jitteriness, and exaggerated tendon reflexes in milder cases to lethargy, stupor, hypotonia in moderate cases, and coma, seizures, and autonomic dysfunction in severe cases of asphyxia G. Multi-system Organ Dysfunction |
| Complications of Asphyxia: Cardiovascular | The acidosis produced during the asphyxiating event decreases myocardial blood flow and depresses ventricular contractility. The neonate could exhibit myocardial dysfunction or even cardiogenic shock. There could be papillary muscle injury, tricuspid insufficiency, right heart failure, or even global heart failure Hypotension is a common complication that offer requires volume support. |
| Complications of Asphyxia: Pulmonary | During the asphyxial event the lungs experience ischemia as blood is shunted away from them to spare the heart and brain. As a result, cellular damage occurs within the alveoli. The cell membranes have been destroyed and fluid leaks into the alveolar space. The infant could experience pulmonary edema and even pulmonary hemorrhage. The type II surfactant producing cells can be destroyed, leading to RDS or shock lung. The pulmonary hypoxia can lead to a persistence of pulmonary hypertension, delay closure of fetal shunts, and right to left shunting. This places the infant at risk for persistent pulmonary hypertension of the newborn. |
| Complications of Asphyxia: Renal | The proximal renal tubule is sensitive to ischemia with a necrosis of the tubular epithelial cells a possibility (Williams, Tan, & Gluckman, 1993). Hypoxemia can lead to degeneration of the tubules or even complete infarction of the nephron. Clinically, the infant could be oliguric to azotemic. Renal failure is very possible depending on the degree of asphyxia. Some studies have shown a worse prognosis overall prognosis, including neurologic prognosis, for infants who experienced renal failure (Williams et al, 1993). Another risk to the kidneys is renal vein thrombosis from the poor circulation and alterations in coagulation that can accompany asphyxia. |
| Complications of Asphyxia: Metabolic | Metabolic acidosis is obviously a problem due to the lactic acid accumulation. Common lab findings include hypoglycemia and hypocalcemia. |
| Complications of Asphyxia: Gastrointestinal | In the body’s effort to spare the heart and brain the blood supply to the GI tract is often reduced in asphyxia. The intestines can sustain cellular damage, which put the infant at a much increased risk for necrotizing entercolitis. Clinically, there may be blood in the stools, an ileus, abdominal distention, and feeding intolerance once feedings have begun. |
| Complications of Asphyxia: Hepatic | The hepatic cells can also sustain injury and clinically the infant could have altered hepatic enzymes, direct hyperbilirubinemia, hypoproteinemia, and abnormalities in the liver dependent clotting factors. Hypoalbuminemia leads to a decreased oncotic pressure and resultant fluid extravasation into the extravascular space. On exam one might see peripheral edema, decreased renal perfusion and decreased urinary output, hypernatremia, and increased blood urea nitrogen. |
| Complications of Asphyxia: Hematology | 1. Asphyxia can cause alterations in platelet function and production. Thrombocytopenia may be seen on lab findings. This should alert the of possibility of a consumptive process which could exacerbate the thrombocytopenia. Asphyxia can also cause a consumption of other coagulation factors increasing the risk for disseminated intravascular coagulopathy (DIC). 2. Bone marrow suppression is also a possibility secondary to asphyxia. This can lead to alterations in WBC production as well as RBC production (anemia is a concern). |
| Complications of Asphyxia: Central Nervous System: Seizures | Damage to the brain can manifest in many forms. One obvious manifestation is seizure activity. Seizure activity greatly increases the metabolic demands of the brain and is associated with a higher risk of neurologic sequelae. The most common form of seizures seen in asphyxiated infants are multifocal clonic seizures. |
| Complications of Asphyxia: Central Nervous System: Cerebral edema | Brain swelling or cerebral edema is a possible consequence of asphyxia. It is thought that the cerebral edema is not necessarily the cause of brain damage, but rather a consequence. The edema is thought to occur from the increased cell membrane permeability in the capillaries which leads to the accumulation of fluid in the extracellular space. The increased swelling is a threat because it can increase intracranial pressure to the point of impeding cerebral blood flow. It reaches it maximum at 36 to 72 hours after severe asphyxia. |
| Complications of Asphyxia: Central Nervous System: Selective neuronal necrosis | Affects the cerebral cerebellar cortex, thalamus, and brain stem. Seen in full term and preterm infants. |
| Complications of Asphyxia: Central Nervous System: Parasagittal neuropathy | Affects parasaggital cortex, subcoritical white matter. Most commonly seen in the term infant. |
| Complications of Asphyxia: Central Nervous System: Status marmoratus of basal ganglia or thalamus | Affects the thalamus, basal ganglia, and cerebral cortex. Seen in full term infants. |
| Complications of Asphyxia: Central Nervous System: Focal or multifocal necrosis | Affects cerebral cortex on one or both sides. Seen in both full and preterm infants. |
| Complications of Asphyxia: Central Nervous System: Periventricular leukomalacia | Affects the periventricular white matter and is seen in premature infants. |
| Management and Therapies: General | Stabilize the infant in the delivery room following guidelines from NRP. The goal is to eliminate the cause of the asphyxia and prevent further damage. |
| Management and Therapies: Cardiovascular | Normalize blood pressure and cardiac output. This may require the use of inotopic medications such as Dopamine or Dobutamine. Depending on the etiology of the asphyxiating event, the infant may have low blood volume. If it is thought the infant has a low blood volume, expansion may be necessary in the form of a transfusion. Be careful as volume expansion in an asphyxiated infant with normal blood volume could be harmful. After sustaining hypoxic-ischemic insult the brain can loose its ability to regulate cerebral vascular tone and the cerebral circulation becomes pressure passive. This must be remembered when giving volume support whether it be in the form of transfusion or fluid bolus to correct hypotension. Placement of an arterial line or umbilical artery catheter will be helpful in monitoring blood pressure. |
| Management and Therapies: Pulmonary | Depending on the degree of injury to the lung tissue and respiratory drive, assisted ventilation may be necessary. It is imperative to maintain normal pH and arterial oxygen and carbon dioxide (CO2) status. Increased CO2 affects the cerebral vascularity by causing vasodilatation. CO2 also promotes a pressure passive cerebral circulation. This vasodilatation increases flow and the risk for hemorrhage. A decreased serum CO2 causes vasoconstriction and compromises cerebral blood flow. Oxygenation must be monitored closely as well. Repeated hypoxic spells should be avoided which could cause further injury. Hyperoxia needs to be avoided as the infant likely will have deficient antioxidant defense mechanisms and excess oxygen could lead to more oxygen free radical damage. Again the placement of an umbilical artery catheter for frequent blood gas analysis is indicated. Transcutaneous CO2 devices and pulse oximetry are helpful methods of non-invasive monitoring of O2 and CO2 status. |
| Management and Therapies: Pulmonary cont'd | If persistent pulmonary hypertension of the newborn (PPHN) is suspected, pre and post ductal oxygen saturations can be monitored. Significant disease can be suspected if the preductal saturation is more than 5% higher than the postductal saturation. Echocardiogram by a cardiologist is confirms the diagnosis. Management of PPHN is beyond the scope of this lecture, but should be reviewed. |
| Management and Therapies: Renal | Anticipate renal failure and provide appropriate fluids to replace insensible water losses and urine losses. Maintain adequate renal blood flow, this may require intravascular fluid boluses and low dose dopamine infusion. Careful measurement of weight, input, output, and vital signs are imperative. If renal function is questioned, a fluid challenge or diuretic could be given. Serum chemistries need to be followed regularly. Hyperkalemia and hyponatremia may be present. Hyponatremia may be the first sign of the syndrome of inappropriate antidiuretic hormone (SIADH). Treatment for this includes fluid restriction, not sodium replacement . |
| Management and Therapies: Metabolic | Correction of metabolic acidosis is foremost. Correction of the etiology is imperative. Sodium bicarbonate administration may be necessary if acidosis is severe. Hypoglycemia and hypocalcemia must be monitored for and corrected as necessary. Hypoglycemia is detrimental to the brain and hyperglycemia has been shown to worsen cerebral damage. Thermoregulation cannot be overlooked and maintenance of a neutral thermal environment is required. |
| Management and Therapies: Gastrointestinal and Hepatic | Due to the risk for NEC, enteral feedings may be delayed days to even a week depending on the degree of the asphyxia. When feedings are begun, small volumes are recommended with daily advancements. Maintenance fluids with adequate nutrition need to be ongoing. Administration of 5% or 25% albumin may be necessary and depends on vascular integrity. |
| Management and Therapies: Hematology | If the degree of thrombocytopenia is severe, the infant may require a platelet transfusion (10cc/kg). If the infant is in DIC and has abnormal PT, PTT, and fibrinogen levels, correction may require blood products. Fresh frozen plasma (FFP) administration is used to correct PT/PTT abnormalities and cryoprecipitate is used to correct low fibrinogen. Anemia may be an issue if the infant suffers from acute blood loss or bone marrow suppression, which can accompany asphyxia. |
| Management and Therapies: Central Nervous System | Treatment is aimed at preventing or controlling seizures. Phenobarbital is recommended at the onset of seizure activity with a loading dose of 10 to 20 mg/kg and maintenance doses of 2 to 5 mg/kg/d. Obtaining an EEG can be helpful in diagnosing subclinical seizures, aids in determining length of anticonvulsant therapy, and assists in predicting outcome. Maintenance of normal blood pH, oxygen, and carbon dioxide levels is crucial to avoid further injury. Abrupt changes in the cerebral vasculature can be dangerous, this requires attention to CO2 levels and systemic blood pressure regulation. Cerebral edema with the resultant increased intracranial pressure is a threat in the asphyxiated infant. Treatments for cerebral edema have included fluid restriction, steroids, and mannitol administration. Currently, fluid restriction seems to be the best supported in the literature |
| Experimental Agents | Brain hypothermia Oxygen free radical inhibitors and scavengers Excitatory amino acid antagonists Calcium channel blockers Inhibitors of nitric oxide production Monoialogangliosides Growth factors Glucocorticosteroids |
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