Systemic effects of perinatal asphyxia
- Lisa M Adcock, MD
Lisa M Adcock, MD
- Clinical Assistant Professor of Pediatrics
- Texas A&M College of Medicine
- Ann R Stark, MD
Ann R Stark, MD
- Professor of Pediatrics
- Vanderbilt University School of Medicine
Perinatal asphyxia results from compromised placental or pulmonary gas exchange. This disorder can lead to hypoxia (lack of oxygen) and hypercarbia (increased carbon dioxide levels) in the blood. Severe hypoxia results in anaerobic glycolysis and lactic acid production first in the peripheral tissues (muscle and heart) and then in the brain. Ischemia (lack of sufficient blood flow to all or part of an organ) is both a cause and a result of hypoxia. Hypoxia and acidosis can depress myocardial function, leading to hypotension and ischemia. Ischemia can impair oxygen delivery, causing further compromise, as well as disrupt delivery of substrate and removal of metabolic and respiratory by-products (eg, lactic acid, carbon dioxide).
The systemic complications of perinatal asphyxia are reviewed here. Hypoxic-ischemic encephalopathy (HIE), including pathogenesis, pathology, diagnosis, prognosis, and treatment, is discussed elsewhere. (See "Etiology and pathogenesis of neonatal encephalopathy" and "Clinical features, diagnosis, and treatment of neonatal encephalopathy".)
TIMING OF INJURY
Asphyxia can occur before, during, or after birth. Based on a review of multiple studies that have examined the temporal relationship between obstetric events and neonatal outcomes, predominantly hypoxic-ischemic encephalopathy (HIE) in term infants, the proportion of conditions that occurs in each time period can be estimated .
Antepartum events, such as maternal hypotension or trauma, account for 4 to 20 percent of cases. Intrapartum events, such as placental abruption or umbilical cord prolapse, are seen in 56 to 80 percent. Evidence of intrapartum disturbance (eg, meconium-stained amniotic fluid or severe fetal heart rate abnormalities) occurs in 10 to 35 percent, usually in association with an antenatal risk factor, such as diabetes mellitus, preeclampsia, or intrauterine growth restriction (IUGR). In approximately 10 percent of cases, a postnatal insult occurs, usually caused by severe cardiopulmonary abnormalities or associated with prematurity.
However, the timing of injury often is difficult to establish for an individual infant, in part because antepartum and intrapartum events may not lead to signs that are detectable in the fetus. In addition, a fetus who has suffered an antepartum insult may be at increased risk of incurring further intrapartum injury.
- Volpe JJ. Hypoxic-ischemic encephalopathy: Clinical aspects. In: Neurology of the Newborn, 5th ed, Saunders Elsevier, Philadelphia 2008. p.400.
- Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet 2005; 365:663.
- Shankaran S, Laptook AR, Ehrenkranz RA, et al. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med 2005; 353:1574.
- Azzopardi DV, Strohm B, Edwards AD, et al. Moderate hypothermia to treat perinatal asphyxial encephalopathy. N Engl J Med 2009; 361:1349.
- Levene MI, deVries LS. Hypoxic-ischemic encephalopathy. In: Fanaroff & Martin's Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, 9th ed, Martin RJ, Fanaroff AA, Walsh MC (Eds), Elsevier, St.Louis 2011. p.952.
- Kluckow M. Functional echocardiography in assessment of the cardiovascular system in asphyxiated neonates. J Pediatr 2011; 158:e13.
- Wei Y, Xu J, Xu T, et al. Left ventricular systolic function of newborns with asphyxia evaluated by tissue Doppler imaging. Pediatr Cardiol 2009; 30:741.
- Matter M, Abdel-Hady H, Attia G, et al. Myocardial performance in asphyxiated full-term infants assessed by Doppler tissue imaging. Pediatr Cardiol 2010; 31:634.
- Möller JC, Thielsen B, Schaible TF, et al. Value of myocardial hypoxia markers (creatine kinase and its MB-fraction, troponin-T, QT-intervals) and serum creatinine for the retrospective diagnosis of perinatal asphyxia. Biol Neonate 1998; 73:367.
- Montaldo P, Rosso R, Chello G, Giliberti P. Cardiac troponin I concentrations as a marker of neurodevelopmental outcome at 18 months in newborns with perinatal asphyxia. J Perinatol 2014; 34:292.
- Szymankiewicz M, Matuszczak-Wleklak M, Hodgman JE, Gadzinowski J. Usefulness of cardiac troponin T and echocardiography in the diagnosis of hypoxic myocardial injury of full-term neonates. Biol Neonate 2005; 88:19.
- Costa S, Zecca E, De Rosa G, et al. Is serum troponin T a useful marker of myocardial damage in newborn infants with perinatal asphyxia? Acta Paediatr 2007; 96:181.
- Rajakumar PS, Vishnu Bhat B, Sridhar MG, et al. Electrocardiographic and echocardiographic changes in perinatal asphyxia. Indian J Pediatr 2009; 76:261.
- 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.
- Selewski DT, Jordan BK, Askenazi DJ, et al. Acute kidney injury in asphyxiated newborns treated with therapeutic hypothermia. J Pediatr 2013; 162:725.
- Durkan AM, Alexander RT. Acute kidney injury post neonatal asphyxia. J Pediatr 2011; 158:e29.
- Karlowicz MG, Adelman RD. Nonoliguric and oliguric acute renal failure in asphyxiated term neonates. Pediatr Nephrol 1995; 9:718.
- Gupta BD, Sharma P, Bagla J, et al. Renal failure in asphyxiated neonates. Indian Pediatr 2005; 42:928.
- Essajee F, Were F, Admani B. Urine neutrophil gelatinase-associated lipocalin in asphyxiated neonates: a prospective cohort study. Pediatr Nephrol 2015; 30:1189.
- Oncel MY, Canpolat FE, Arayici S, et al. Urinary markers of acute kidney injury in newborns with perinatal asphyxia (.). Ren Fail 2016; 38:882.
- Banupriya C, Ratnakar, Doureradjou P, et al. Can urinary excretion rate of malondialdehyde, uric acid and protein predict the severity and impending death in perinatal asphyxia? Clin Biochem 2008; 41:968.
- Thibeault DW, Hall FK, Sheehan MB, Hall RT. Postasphyxial lung disease in newborn infants with severe perinatal acidosis. Am J Obstet Gynecol 1984; 150:393.
- Faix RG, Viscardi RM, DiPietro MA, Nicks JJ. Adult respiratory distress syndrome in full-term newborns. Pediatrics 1989; 83:971.
- Pfenninger J, Tschaeppeler H, Wagner BP, et al. The paradox of adult respiratory distress syndrome in neonates. Pediatr Pulmonol 1991; 10:18.
- Khammash H, Perlman M, Wojtulewicz J, Dunn M. Surfactant therapy in full-term neonates with severe respiratory failure. Pediatrics 1993; 92:135.
- Berseth CL, McCoy HH. Birth asphyxia alters neonatal intestinal motility in term neonates. Pediatrics 1992; 90:669.
- Akinbi H, Abbasi S, Hilpert PL, Bhutani VK. Gastrointestinal and renal blood flow velocity profile in neonates with birth asphyxia. J Pediatr 1994; 125:625.
- Andrews DA, Sawin RS, Ledbetter DJ, et al. Necrotizing enterocolitis in term neonates. Am J Surg 1990; 159:507.
- Karlsson M, Blennow M, Nemeth A, Winbladh B. Dynamics of hepatic enzyme activity following birth asphyxia. Acta Paediatr 2006; 95:1405.
- Rainaldi MA, Perlman JM. Pathophysiology of Birth Asphyxia. Clin Perinatol 2016; 43:409.
- Castle V, Andrew M, Kelton J, et al. Frequency and mechanism of neonatal thrombocytopenia. J Pediatr 1986; 108:749.
- Christensen RD, Baer VL, Yaish HM. Thrombocytopenia in late preterm and term neonates after perinatal asphyxia. Transfusion 2015; 55:187.
- Bauman ME, Cheung PY, Massicotte MP. Hemostasis and platelet dysfunction in asphyxiated neonates. J Pediatr 2011; 158:e35.
- TIMING OF INJURY
- RISK FACTORS
- Antepartum conditions
- Intrapartum events
- Postnatal disorders
- Fetal biophysical profile
- ORGAN INVOLVEMENT
- MYOCARDIAL DYSFUNCTION
- Clinical features
- RENAL DYSFUNCTION
- PULMONARY DISORDERS
- Pulmonary edema
- Acute respiratory distress syndrome
- GASTROINTESTINAL DYSFUNCTION
- Feeding intolerance
- Necrotizing enterocolitis
- - Management
- Hepatic dysfunction
- HEMATOLOGIC DISORDERS
- SUMMARY AND RECOMMENDATIONS