or arterial wall abnormalities are due to vascular malformations, thickening
of the intima, or obliterative arteritis. Obliterative arteritis is probably
the cause of cerebral infarcts in infants of cocaine-addicted mothers.
Extramural abnormalities such as neoplasms can produce cerebral infarcts
but they most frequently produce intracranial bleeding. Asphyxia may produce
cerebral infarcts by a combination of endomural and mural factors. Neonates
with cerebral infarct should be evaluated by obtaining MRI and MRA of
the brain, carotid ultrasonogram, echocardiogram, EKG, CBC with differential
and platelets, prothrombin time, partial thromboplastin time, fibrinogen
splitting products, proteins S and C activity levels, antithrombine-III
activity, antiphospholipid antibody, urine for homocysteine, and factor-V
Leidenpolymerase chain reaction
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diagnosis of hypoxic-ischemic encephalopathy should be based on clinical
evidence of encephalopathy and perinatal asphyxia. Perinatal asphyxia
is diagnosed in the presence of 3 or more of the following findings: (1)
intrapartum distress (bradycardia with a heart rate of less than 100 beats
per minute, late decelerations, or absence of beat-to-beat variability);
(2) thick meconium-stained amniotic fluid, (3) an APGAR score of 6 or
less at 5 minutes, (4) a need for resuscitation for more than 1 minute
with positive pressure ventilation and oxygen immediately after birth,
and (5) an arterial pH value of 7.20 or less or a base deficit of at least
14 mmol per liter within the first hour after birth.
A minimal degree of encephalopathy produces lethargy and mild hypotonia
with superimposed jitteriness. These findings, if lasting less than 24
hours, are very common after a traumatic delivery. Severe hypoxic-ischemic
encephalopathies manifest as coma. Neonates with severe hypoxic-ischemic
encephalopathies are hypotonic and have evidence of brainstem dysfunction.
Asphyxia should be diagnosed if an event of hypotension and hypoxia is
documented by clinical or laboratory findings. The presence of multi-organ
involvement (high blood-urea nitrogen, creatine, and creatine phosphokinase)
is often present in asphyxiated neonates. The degree of acidemia reflects
the severity of the asphyxia. Computed tomography or MRI of the brain
may initially demonstrate brain edema and, after 14 days, laminar cortical
necrosis and status marmoratus (Figure 55.1).
Hypoxic ischemic encephalopathy. [A] T1- weighted
sagittal image of the brain demonstrates laminar necrosis and diffuse
hyperintensity of the basal ganglia and thalami. [B] T1-
weighted axial image of the brain demonstrates laminar necrosis (especially
in the occipital region) and diffuse hyperintensity of the thalami.