Definition:
Occurs when placental or pulmonary gas exchange to a fetus/newborn is compromised, resulting in hypoxia in the blood
Implications:
Hypoxia forces fetal cells to undergo anaerobic respiration which produces less energy for cells and lactic acid as a byproduct. Energy produced from anaerobic respiration cannot properly supply fetal/newborn tissue therefore cell function becomes compromised. The tissues affected first include the heart, muscle, and brain. Myocardial function eventually becomes depressed and hypotension results in end organ damage to a variety of systems. When oxygen is reinstituted into the blood, reactive oxygen species can further damage tissues, this is known as reperfusion injury (1).
Terminology:
When discussing the possible causes of asphyxia it can be helpful to think about the following time frames.
- Antepartum: period before labor
- Perinatal: period shortly before and after birth (from 29 wks gestation to 4 wks postpartum)
- Intrapartum: period around delivery and birth
Main Causes of Hypoxia:
- Antepartum (4-20% of cases): compromise placental gas exchange
a. Maternal hypotension
b. Trauma
c. Severe anemia
- Perinatal (10% of cases): compromise pulmonary gas exchange in newborn
a. Prematurity- decreased surfactant
b. Severe cardiopulmonary abnormalities
- Intrapartum (56-80% of cases): compromise placental gas exchange
a. Placental abruption- separation of placenta from lining of
uterus
b. Umbilical cord prolapse- cord precedes fetus exit from uterus
Complications from Hypoxia:
Hypoxia can damage every organ system in a similar way as hypotension does during shock.
Brain:
Hypoxic-ischemic encephalopathy (HIE) is considered the most serious complication of perinatal asphyxia.
HIE describes CNS damage that results from hypoxia. Important symptoms include abnormal states of consciousness (either hyperalert, irritable, lethargic or obtunded), respiratory or feeding difficulties, poor tone and seizures (2). CT and MRI imaging can help determine the type of brain injury sustained, the timing that it occurred and some prognostic indication (3). Repeating a neurological exam is an important tool when evaluating symptoms and their progression. Treatment should take place in an ICU and is aimed at maintaining adequate ventilation, brain and organ perfusion, metabolic status and preventing cerebral edema and seizures. Therapeutic hypothermia has been shown to improved survivals and outcomes at 18 months of age (4). Associated neurologic morbidities include learning disabilities, ADD, cerebral palsy, epilepsy, visual impairment and significant cognitive and developmental disorders. Prognosis depends on clinical predictors:
Mild symptoms of HIE include hyperexcitability, normal tone and no seizures. These infants have a high probability of being normal at follow-up (5).
Moderate symptoms of HIE include hypotonia, decreased movements and possibly seizures. These infants have a 20-35% risk of neurologic morbidity (6).
Severe symptoms of HIE include stuporous affect, flaccidness, absent primitive reflexes and seizures. These infants have a 75% risk of dying in the neonatal period and those that survive will have significant neurologic morbidities (7).
Heart:
Myocardial dysfunction results secondary to tissue ischemia.
Even though this is generally a transient effect it can result in cardiogenic shock and death. Troponin T levels are specific to cardiac damage and can correlate to the severity of asphyxia. Imaging modalities can show signs of heart failure. A CXR can shows cardiomegaly, an echocardiogram can reveal a decreased systolic ejection fraction and EKG can confirm ischemia. Treatment is supportive, pay special attention to metabolic abnormalities and mechanically ventilate if needed (8).
Kidneys:
Acute kidney injury (AKI) commonly accompanies perinatal asphyxia.
Severe hypoxia results in diffuse tubular dysfunction and impairs the reabsorption of water and electrolytes by decreasing the GFR. Creatinine values >1-1.5 mg/dL indicate AKI. Monitoring urine output and creatinine levels can provide insight into the degree of AKI. Other important lab tests include UA, urine electrolytes, FeNa, and a CBC. An ultrasound can also be helpful. Treatment of AKI includes maintaining fluid and electrolyte balances until recovery (9,10).
Lung:
Complications include pulmonary edema and acute respiratory distress syndrome (ARDS).
Pulmonary edema: Myocardial dysfunction causes backflow of fluid into the lungs. Symptoms include cyanosis, nasal flaring, tachypnea and crackles on exam. Treatment includes oxygen supplementation, ventilation and addressing cardiac dysfunction (11).
ARDS: Increased permeability of the pulmonary capillary beds to plasma proteins inactivates surfactant in the lungs. This results in severe respiratory distress and cyanosis. Chest XR reveals reduced lung volumes and diffuse bilateral opacities. Treatment requires oxygen supplementation and mechanical ventilation with PEEP until recovery (12).
GI:
Feeding intolerance and necrotizing enterocolitis (NEC) are common complications.
Feeding intolerance results from a disruption in intestinal neuronal and motor control. Symptoms include abdominal distention, delayed gastric emptying as well as gagging. Treatment involves delaying feeds for 5-7 days until intestinal neuronal and motor control recovers (13).
NEC is ischemic necrosis of the intestinal mucosa secondary to decreased cardiac output. The incidence increases with decreasing gestational age, meaning premature newborns with hypoxia are at the highest risk. Symptoms include abdominal distention and bloody stools. Abdominal XR shows diagnostic pneumatosis intestinalis, which refers to gas cysts in the bowel wall. Treatment is required immediately and includes fluids, antibiotics, transfusions if necessary and surgery. Monitor recovery with abdominal XRs and CBCs( 14,15).
Depending on the degree of neurologic insult, feeding via an NG, NJ or G-tube to optimize nutrition is often common when the damage is severe.
References:
1. http://www.uptodate.com/contents/clinical-features-diagnosis-and-treatme...
2. How much of neonatal encephalopathy is due to birth asphyxia? Nelson KB, Leviton A. Am J Dis Child. 1991;145(11):1325.
3. Origin and timing of brain lesions in term infants with neonatal encephalopathy.Cowan F, Rutherford M, Groenendaal F, Eken P, Mercuri E, Bydder GM, Meiners LC, Dubowitz LM, de Vries LS. Lancet. 2003;361(9359):736.
4. Hypothermia for neonatal hypoxic ischemic encephalopathy: an updated systematic review and meta-analysis.Tagin MA, Woolcott CG, Vincer MJ, Whyte RK, Stinson DA. Arch Pediatric Adolescent Med. 2012;166(6):558.
5. Birth asphyxia: incidence, clinical course and outcome in a Swedish population. Thornberg E, Thiringer K, Odeback A, Milsom IActa Paediatr. 1995;84(8):927
6. Hypoxic-ischemic encephalopathy in term neonates: perinatal factors and outcome.Finer NN, Robertson CM, Richards RT, Pinnell LE, Peters KLJ Pediatrics. 1981;98(1):112.
7. Acute neonatal morbidity and long-term central nervous system sequelae of perinatal asphyxia in term infants.Shankaran S, Woldt E, Koepke T, Bedard MP, Nandyal R Early Hum Dev. 1991;25(2):135.
8. Volpe JJ. Hypoxic-ischemic encephalopathy: Clinical aspects. In: Neurology of the Newborn, 5th ed, Saunders Elsevier, Philadelphia 2008. p.400.
9. Seri, I, Evans, J, Tulassay, T. Renal insufficiency and acute renal failure. In: Avery's Diseases of the Newborn, 7th ed, Taeusch, HW, Ballard, RA (Eds), WB Saunders, Philadelphia 1998, p. 1158.
10. Renal failure in asphyxiated neonates.Gupta BD, Sharma P, Bagla J, Parakh M, Soni JP. Indian Pediatrics. 2005;42(9):928.
11. Postasphyxial lung disease in newborn infants with severe perinatal acidosis.
12. Adult respiratory distress syndrome in full-term newborns.Faix RG, Viscardi RM, DiPietro MA, Nicks JJPediatrics. 1989;83(6):971.
13. Birth asphyxia alters neonatal intestinal motility in term neonates .Berseth CL, McCoy HH. Pediatrics. 1992;90(5):669.
14. The radiology of necrotizing enterocolitis.Buonomo C. Radiol Clin North Am. 1999;37(6):1187.
15. Necrotizing enterocolitis in term neonates.Andrews DA, Sawin RS, Ledbetter DJ, Schaller RT, Hatch EI. Am J Surg. 1990;159(5):507.