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the lungs, liver, adrenal glands, CNS, skin, eyes, and mouth. Approximately 86% to 90% of
herpes simplex virus transmission occurs during delivery.
Vascular birthmarks may be divided into vascular malformations and vascular tumors
(hemangiomas). Vascular tumors are known as hemangiomas of infancy or infantile
hemangiomas to differentiate them from other vascular tumors and malformations. Localized
superficial hemangiomas tend to manifest early in infancy, and spontaneous resolution without
therapy may occur within several years; the segmental variety is more likely to cause
complications such as ulceration and vital organ compromise and to involve developmental
defects.
Vascular malformations are permanent lesions that are present at birth and are initially flat and
erythematous. The two most common vascular stains are port-wine stains (nevus flammeus)
and transient macular stains such as the stork bite or salmon patch, usually located on the
glabella or nape of the neck. Port-wine lesions are pink, red, or rarely, purple stains of the skin
that thicken, darken, and proportionately enlarge as the child grows.
Brachial plexus injury results from forces that alter the normal position and relationship of the
arm, shoulder, and neck. Erb palsy (Erb-Duchenne paralysis) is caused by damage to the
upper plexus and usually results from stretching or pulling away of the shoulder from the
head, as might occur with shoulder dystocia or with a difficult vertex or breech delivery. The
arm hangs limp alongside the body. The shoulder and arm are adducted and internally rotated.
The elbow is extended, and the forearm is pronated, with the wrist and fingers flexed; a grasp
reflex may be present because finger and wrist movement remain normal.
The less common lower plexus palsy, or Klumpke palsy, results from severe stretching of the
upper extremity while the trunk is relatively less mobile. In lower plexus palsy, the muscles of
the hand are paralyzed, with consequent wrist drop and relaxed fingers.
Hyperbilirubinemia is an excessive level of accumulated bilirubin in the blood and is
characterized by jaundice, or icterus, a yellowish discoloration of the skin and other organs.
Hyperbilirubinemia may result from increased unconjugated or conjugated bilirubin. The
unconjugated form is the type most commonly seen in newborns.
Hour-specific serum bilirubin levels to predict newborns at risk for rapidly rising levels are
used for monitoring healthy neonates at more than 35 weeks of gestation before discharge
from the hospital. Using a nomogram with three designated risk levels (high, intermediate, or
low risk) of hour-specific total serum bilirubin values assists in the determination of which
newborns might need further evaluation before and after discharge.
The primary goal in the treatment of hyperbilirubinemia is to prevent bilirubin
encephalopathy, a term that describes varying degrees of CNS damage resulting from the
deposition of unconjugated bilirubin in brain cells. Kernicterus describes the yellow staining
of the brain cells that may result in bilirubin encephalopathy. The damage occurs when the
serum concentration reaches toxic levels, regardless of cause.
The main treatment of hyperbilirubinemia involves the use of phototherapy, which consists
of the application of fluorescent light to the infants exposed skin.
Hemorrhagic disease of the newborn (HDN) is characterized by abnormally rapid
destruction of red blood cells (RBCs) as a result of blood incompatibility between the mother
Copyright 2015, 2011, 2007, 2003, 1999 by Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
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and fetus. The major causes of increased erythrocyte destruction are isoimmunization
(primarily RhD) and ABO incompatibility.
With ABO incompatibility, the incompatibility is between a mother with O blood group and
an infant with A or B blood group; hemolysis is more commonly caused by anti-A than anti-B.
In Rh incompatibility the problem occurs when the Rh-positive fetuss blood cells pass into
the circulation of the Rh-negative mother in sufficient quantities to produce anti-Rh
antibodies, which in turn may enter the fetal circulation and cause fetal RBC hemolysis.
In the most severe form of erythroblastosis fetalis (hydrops fetalis), the progressive
hemolysis causes fetal hypoxia; cardiac failure; generalized edema (anasarca); hydrops; and
effusions into the pericardial, pleural, and peritoneal spaces. The fetus may be delivered
stillborn or in severe respiratory distress. Maternal Rh immunoglobulin (RhIg) administration,
early intrauterine detection of fetal anemia by ultrasonography (serial Doppler assessment of
the peak velocity in the fetal middle cerebral artery), and subsequent treatment by fetal blood
transfusions or high-dose intravenous immunoglobulins have dramatically improved the
outcome of affected fetuses.
Cleft lip (CL) results from incomplete fusion of the embryonic structures surrounding the
primitive oral cavity; the cleft may be unilateral or bilateral and is often associated with
abnormal development of the external nose, nasal cartilages, nasal septum, and maxillary
alveolar ridges. Cleft palate (CP) occurs when the primary and secondary palatine plates fail
to fuse during embryonic development. CPs may involve only the soft palate or may extend
into the hard palate. The cleft may be unilateral or bilateral and may occur in conjunction with
cleft lip or as an isolated cleft.
Major nursing challenges with infants born with either CL or CP involve feeding. Treatment
of children with CL or CP is surgical and involves the craniofacial multidisciplinary team.
Surgical correction of the CL usually occurs around 2 to 3 months of life, and postoperative
care centers on protection of the suture line. CP surgical closure is typically performed at 6 to
12 months before the child develops compensatory speech patterns. Postoperatively the palate
is protected by feeding the child with a soft-tip (like a nipple) sippy cups, an open cup, an
oropharyngeal syringe, or specialized bottles with soft tubing. Long-term follow up of CP is
necessary to promote optimal speech and prevent abnormal dentition.
Pierre Robin sequence (PRS) is a defect characterized by retroposition of the tongue and
mandible, which often results in neonatal respiratory and feeding problems. The tongue may
be large (glossoptosis) and frequently falls over the neonates airway, causing occlusion and
respiratory distress.
Hypoglycemia is present when the newborns blood glucose concentration is lower than the
bodys requirement for cellular energy and metabolism. However, the precise definition of
hypoglycemia for every newborn in regard to gestational age, birth weight, metabolic needs,
and illness or wellness state remains unknown. Some experts suggest that a serum glucose
below 45 mg/dl in a healthy term infant without risk factors such as small for gestational age
(SGA) or infant of a diabetic mother (IDM) represents hypoglycemia, yet absolute values
defining hypoglycemia in all infants remain controversial.
Copyright 2015, 2011, 2007, 2003, 1999 by Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.