• Coexistence of hypoxemia, hypercapnia and metabolic acidosis is defined as asphyxia.
Risk factors for perinatal asphyxia
Associated with the fetus
Pre / Postmaturity
Intrauterine growth retardation
Multiple pregnancy
severe pulmonary disease
Infection
Congenital heart disease
Associated with the mother
Diabetes
Hypo / Hypertension (Preeclampsia)
Anemia
Isoimmunization
Advanced maternal age (>35)
Associated with pregnancy/birth
polyhydramnios
Antepartum bleeding
Cord compression/prolapse
placental insufficiency
abnormal presentation
Neuropathology
• Insufficiency of ATP production with anaerobic energy production effort in CNS causes increase in intracellular water, sodium and calcium, neuron damage and development of encephalopathy.
• Brain edema and brain necrosis are the leading findings of neuropathology.
• A significant increase is also observed in the excitatory amino acids aspartate and glutamate and nitric oxide secretion in the CSF of asphyctic infants.
• Disruption of autoregulation, hypo and hypertension cause further aggravation of the picture.
Diagnosis
• A careful history and neurological examination are important in diagnosis.
• APGAR score of 6 or lower at the 5th minute is an important finding in the diagnosis of asphyxia.
• The greatest risk and worst prognosis is when severe acidosis (pH<6.7) (90% deaths) and base deficit > 25 mmol/L (72% deaths).
• Significant voltage drop and isoelectric line in amplitude integrated EEG (aEEG) indicate diffuse cortical neuron necrosis.
• Diffusion weight MRI has high sensitivity and specificity in showing the damaged area and location of lesions.
• Hyperammonemia, increase in brain specific creatine kinase (CK-BB) in blood and CSF, increase in blood uric acid, AST, erythropoietin, beta endorphin, lactate, LDH, neuron specific enolase are seen in severe perinatal asphyxia.
Organ and system pathology in perinatal asphyxia
cerebral
• Hypoxic ischemic encephalopathy
• Brain edema
• Infarct
• intracranial hemorrhage
• seizures
• Hypotonia/Hypertonia
Renal
Acute tubular or cortical necrosis
Gastrointestinal System
• Perforation
• Hemorrhagic ulceration
• Necrosis
Cardiovascular system
Myocardial ischemia, papillary muscle necrosis, tricuspid regurgitation, hypotension, weak contractility
Pulmonary
• Pulmonary hemorrhage
• Pulmonary hypertension
• Respiratory distress syndrome
Hematological
Disseminated intravascular coagulation (DIC)
Metabolic
• Hyponatremia / Inappropriate ADH release syndrome
• Hypoglycemia
• Hypocalcemia
• Metabolic acidosis
• Myoglobinuria
Skin
Subcutaneous fat necrosis
Treatment
• Ensuring adequate ventilation and keeping blood gases within optimal limits. Since vasodilation and bleeding in hypercarbia and cerebral blood flow decrease in hypocarbia, ischemic damage occurs.
• Total body or head cooling (therapeutic hypothermia): In the first 6 hours of life, the neurological prognosis is significantly improved by keeping the body temperature controlled at 33.5 °C for 72 hours. At least babies born with asphyxia should not be overheated. It is the best known treatment method today. It has been shown to improve mortality and neurodevelopmental status at 18 months.
• Treatment of hypothermia may cause thrombocytopenia (usually not bleeding), bradycardia, and subcutaneous fat necrosis. Although it is theoretically thought to affect drug metabolism and cause QT prolongation, these effects have not been observed clinically.
• The first choice in the treatment of convulsions is phenobarbital. Phenytoin is especially preferred in patients with liver damage due to asphyxia.
• Allopurinol
• Calcium channel blockers
Poor prognosis in HIE
• pH<6,7 in cord blood gas
• APGAR (5. Min)<= 3
• Base minus <-20-25 mmol/L
• Low APGAR 20th Minute score
• Still no spontaneous breathing at the 20th minute
• Stage 3
• Finding severe abnormalities on cranial MRI and aEEG
• Severe basal ganglia and thalamus damage
