Michael J. Acarregui, MD
Peer Review Status: Internally Peer Reviewed

The term asphyxia infers an impairment of gas exchange resulting in a fall in PO2 and a rise in PCO2. Degrees of asphyxia exist, varying from total asphyxia, characterized by anoxia and extremes of hypercarbia, to the more commonly encountered situation of partial asphyxia, involving hypoxia and moderate elevations of PCO2. Asphyxial events may occur in utero, at birth, or during postnatal life. Ischemia is often an integral component of asphyxia. Thus the term hypoxia-ischemia is often used interchangeably with asphyxia. A gold standard definition of asphyxia does not exist, and different criteria have been used to diagnose asphyxia including: fetal heart rate patterns, meconium stained amniotic fluid, Apgar scores, umbilical artery pH, need for resuscitation at birth, seizures, electroencephalographic abnormalities, and the development of a clinical neurologic syndrome. At birth there is often insufficient information to readily determine if an asphyxial insult has occurred, and if it has occurred, whether any organ system dysfunction has resulted. For example, seizures may not occur immediately after birth and a clinical neurologic syndrome may evolve over 2-3 postnatal days. This may pose potential problems since inappropriate triage of infants may occur and result in delay in management when obvious problems develop. In spite of these considerations it is critical to note that asphyxial insults in the perinatal period do not account for the majority of infants with brain injury in early childhood.

Perinatal asphyxia leads to multi-organ system dysfunction. Virtually any organ system can be affected, and care in the nursery should be oriented to determining the presence or absence of dysfunction of critical organ systems. Cardiovascular involvement may include alterations in blood volume, redistribution of cardiac output and a syndrome of transient myocardial dysfunction. Neurologic involvement is characterized by the evolution of a characteristic hypoxic-ischemic encephalopathy of which seizures may be a part. The Sarnat stages (I-III) of post-hypoxic encephalopathy represent a convenient description to characterize the extent of neurologic involvement and important features are listed in the table.

Salient Features of Sarnat Stages of Post-hypoxic Encephalopathy
  Stage I Stage II Stage III
Level of consciousness hyperalert lethargic or obtunded stuporous
Neuromuscular control
Muscle Tone
Posture
normal
mild distal
flexion
mild hypotonia
strong distal
flexion
flaccid
intermittent
decerebration
Stretch reflexes overactive overactive decrease or absent
Complex Reflexes
Suck
Moro

weak
strong; low threshold

weak or absent
weak:incomplete high threshold

absent
absent
Autonomic Function generalized
sympathetic
generalized
parasympathetic
both system
depressed
Seizures none common; focal or
multifocal
uncommon

Metabolic involvement may include hypocalcemia, hyponatremia (as a result of inappropriate ADH secretion or direct renal injury), and alterations in glucose metabolism. Pulmonary involvement may include persistent pulmonary hypertension, aspiration syndromes (usually meconium) and asphyxial lung disease (rare). Direct renal injury may occur leading to acute tubular necrosis. Ischemic bowel disease may occur presumably as a result of the redistribution of cardiac output (dive reflex response). Less commonly, hematologic alterations (thrombocytopenia and DIC) and subcutaneous fat necrosis occur. Clinical care of these infants should be directed at surveillance and management of specific organ system dysfunction. Fluid management should be cautious.