Nursing Care Aspects for High Risk newborn

By hidayatullah khan

KMU

Birth injuries

Definition:

The term birth injury is used to denote: avoidable and unavoidable mechanical, hypoxic and ischemic injury affecting the infant during delivery.

• Birth injuries may result from :
• Inappropriate or deficient medical skill or attention.
• They may occur, despite skilled and competent obstetric care.

Birth Injuries

• Soft Tissue Injuries (Abrasions, Bruising, Fat Necrosis, Lacerations)
• Extracranial Bleeding (Caput succedaneum, Cephalhematoma, or Subgaleal Hematoma)
• Intracranial Bleeding (Subarachnoid, Epidural, Subdural, Cerebral,)
• Nerve Injuries (Facial and Cervical Nerve Roots, Horner Syndrome, Recurrent Laryngeal Nerve)
• Fractures (Clavicle, Humerus, Femur, Skull)
• Dislocations (hip, shoulder)
• Torticollis (Sternocleidomastoid injury)
• Eye Injuries (Subconjunctival and Retinal Hemorrhage)
• Solid Organ Injury (liver, spleen, kidney, adrenal glands)

Predisposing factors

• Primigravida
• Cephalopelvic disproportion
• Small maternal stature
• maternal pelvic anomalies
• Prolonged or rapid labor
• Arrest of descent of presenting fetal part
• Oligohydramnios
• Resuscitation with CPR

• Abnormal presentation (breech/face)
• Use of forceps or vacuum extraction
• VLBW infant or extreme prematurity
• Macrosomia
• Large fetal head
• Fetal anomalies
• Fetal neuromuscular disease
• Dystocia

Incidence

• Has been estimated at 2-7/1,000 live births.

Erythema, abrasions, ecchymoses,�

• Of facial or scalp soft tissues may be seen after forceps or vacuum-assisted deliveries.
• Their location depends on the area of application of the forceps.
• Subconjunctival ,retinal hemorrhages and petechiae of the skin of the head and neck.
• All are secondary to a sudden increase in intra thoracic pressure during passage of the chest through the birth canal.
• Parents should be assured that they are temporary and the result of normal hazards of delivery.

Molding

• Molding of the head and overriding of the parietal bones are frequently associated with caput succedaneum and become more evident after the caput has receded but disappear during the first weeks of life.
• Rarely, a hemorrhagic caput may result in shock and require blood transfusion.

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Caput succedaneum

• ecchymotic, edematous swelling of the soft tissues of the scalp.
• It may extend across the midline and across suture lines.
• The edema disappears within the first few days of life.

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Caput succedaneum

• Analogous swelling, discoloration, and distortion of the face are seen in face presentations.
• No specific treatment is needed, but if there are extensive ecchymoses, phototherapy for hyperbilirubinemia may be indicated.

Caput Succedaneum

• Common after prolonged labor
• Accumulation of blood/serum above periosteum
• Soft tissue swelling / edema / petechiae / ecchymoses
• Crosses suture lines

Cephalhaematoma

• It is a subperiosteal haematoma most commonly lies over one parietal bone.

It may result from difficult vacuum or forceps extraction .

Management:

- It usually resolves spontaneously.

- Vitamin K 1 mg IM is given.

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Cephalohematoma

• Is a subperiosteal hemorrhage, so it is always limited to the surface of one cranial bone.
• There is no discoloration of the overlying scalp, and swelling is usually not visible until several hours after birth, because subperiosteal bleeding is a slow process.
• An underlying skull fracture, usually linear and not depressed, is occasionally associated with cephalohematoma.
• Most cephalohematomas are resorbed within 2 wk-3 mo, depending on their size.
• They may begin to calcify by the end of the 2nd wk.

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Cephalohematoma

• A sensation of central depression suggesting( but not indicative )of an underlying fracture or bony defect is
• Cephalohematomas require no treatment, although phototherapy may be necessary to ameliorate hyperbilirubinemia.
• Incision and drainage are contraindicated because of the risk of introducing infection in a benign condition.
• A massive cephalohematoma may rarely result in blood loss severe enough to require transfusion.
• It may also be associated with a skull fracture, coagulopathy, and intracranial hemorrhage

Cephalhematoma

Diagnosis and Differential Diagnosis

Intracranial Haemorrhage:

Causes:

1. Sudden compression and decompression of the head as in breech and hurried labour.
2. Marked compression by forceps or in cephalopelvic disproportion.
3. Fracture skull.

Predisposing factors:

• Prematurity due to physiological hypoprothrombinaemia, fragile blood vessels and liability to trauma.
• Blood diseases.

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Intracranial Haemorrhage Sites:

1. Subdural
2. Subarachnoid
3. Intraventricular
4. Intracerebral

The incidence of IVH increases with decreasing birthweight:

1. 60-70% of 500- to 750-g infants and
2. 10-20% of 1,000- to 1,500-g infants

Intracranial Haemorrhage:

Clinical picture:

1- Altered consciousness.

2- Flaccidity.

3- Breathing is absent, irregular and periodic or gasping.

4- Eyes: no movement, pupils may be fixed and dilated.

5- Opisthotonus, rigidity, twitches and convulsions.

6- Vomiting .

7- High pitched cry.   

8- Anterior fontanelle is tense and bulging.

9- Lumbar puncture reveals bloody C.S.F.

Intracranial Haemorrhage

Investigations:

• Ultrasound is of value.
• CT scan is the most reliable.
• MRI

Prophylaxis:

2. Vitamin K: 10 mg IM to the mother in late pregnancy or early in labour.
3. Episiotomy: especially in prematures and breech delivery.
4. Forceps delivery
5. For baby supportive treatment :

Brachial Plexus Palsy:

It is due to over traction on the neck as in:

1. Shoulder dystocia.     
2. After-coming head in breech delivery.

Brachial Plexus Palsy:

1. Erb's palsy:
1. It is the common, due to injury to C5 and C6 roots.
2. The upper limb drops beside the trunk, internally rotated with flexed wrist.

2) Klumpke’s palsy:

• Due to injury to C7 and C8 and 1st thoracic roots.

- It leads to paralysis of the muscles of the hand and weakness of the wrist and fingers.

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(policeman’s or waiter’s tip hand).

Brachial Plexus Palsy

Brachial Plexus Palsy:

Treatment

• Support to prevent stretching of the paralyzed muscles.
• Physiotherapy: massage, exercise and faradic stimulation.

The prognosis

• Depends on whether the nerve was merely injured or was lacerated.
• If the paralysis was due to edema and hemorrhage about the nerve fibers, function should return within a few months;
• If due to laceration, permanent damage may result.

Treatment

• If the paralysis persists without improvement for 3-6 months: neuroplasty, neurolysis, end-to-end anastomosis, or nerve grafting

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PHRENIC NERVE PARALYSIS

• Phrenic nerve injury (3rd, 4th cervical nerves) with diaphragmatic paralysis must be considered when cyanosis and irregular and labored respirations develop.
• Such injuries, usually unilateral, are associated with upper brachial palsy.
• There is no specific treatment: infants should be placed on the involved side and given oxygen if necessary.
• Recovery usually occurs spontaneously by 1-3 months; rarely, surgical plication of the diaphragm may be indicated.

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clavicle fracture

• This bone is fractured during delivery more frequently than any other bone; It is particularly vulnerable when there is:
• Difficulty in delivery of the shoulder in vertex presentations and of
• The extended arms in breech
• The infant characteristically does not move the arm freely on the affected side;
• Crepitus and bony irregularity may be palpated, and
• Discoloration is occasionally visible over the fracture site.
• deliveries.

Treatment

• Treatment, consists of immobilization of the arm and shoulder on the affected side.
• A remarkable degree of callus develops at the site within a week and may be the first evidence of the fracture.
• The prognosis is excellent.

Injuries to spine and spinal cord

• Result from breech deliveries, face presentations
• Upper or mid-cervical region-flaccidity and immobility of the lower limbs, urinary retention may be the first symptom, paralysis of the abdominal wall, intercostal muscles may be affected , sensation is absent over the lower half of the body, constipation.

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Treatment

• Infants affected at birth require basic resuscitative measures
• In case of vertebral fracture-immediate neurosurgical consultation for reduction and relief of cord compression, followed by appropriate immobilization
• Position of paralyzed parts should be changed every 2 hrs, indwelling urinary catheter should be inserted
• Urology consult

Traumatic Nerve & Spinal Cord Injuries

Injuries to intra-abdominal organs

• Rupture of the liver- large infants, IDM,breech
• May appear normal for 1-3 days of life, any infant with shock, abdominal distension, pallor, anemia, and irritability with no evidence of blood loss
• Abdomen is rigid, bluish discoloration of the overlying skin. CT scan may help in diagnosing subcapsular hematoma

Treatment

• Prompt correction of coagulation disorder
• Laparotomy with evacuation of the hematoma and repair of any lacerations
• Any fragmented, liver tissue should be removed
• Blood transfusion and the tamponade of intra-abdominal pressure might be adequate therapy in some infants

Rupture of the spleen

• Large infants in breech position, erythroblastosis, congenital syphilis
• Underlying clotting defect
• Clinical signs of hemoperitoneum and blood loss
• Left upper quadrant mass and medial displacement of the gastric bubble
• Packed cells and exploratory laparotomy
• Attempt to repair and preserve the spleen

Subcapsular liver hemorrhage

RDS

• Respiratory distress syndrome (RDS) is a problem often seen in premature babies. The condition makes it hard for the baby to breathe.
• caused by developmental insufficiency of surfactent production and structural immaturity in the lungs.

Risk factors (High risk group):�e.g: Prematurity and low birth weight.

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Clinical Presentation:��Grade I: (Mild distress): Rapid respiratory rate (tachypnea >60 breaths per minute) + nasal flaring � Grade II: (Moderate distress): GI + intercostals and substernal retractions.�Grade III: (Severe distress): GI + GII + expiratory grunting.�Grade IV: (Advanced distress): GI + GII + GIII + central cyanosis and disturbed consciousness.�

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Respiratory Distress Syndrome - RDS

• Pathophysiology
• Primary absence, deficiency or alteration in the production of surfactant
• Surfactant, atelectasis = lack of gas exchange
• Leads to hypoxia and acidosis which further inhibit surfactant production and causes pulmonary vasoconstriction.
• Clinical manifestations:
• Cyanosis
• Tachypnea
• Nasal flaring
• Retracting
• Apnea

Management of RDS:�A) General:�* Basic support including thermal regulation and parentral nutrition and medications (antibiotics).� * Oxygen administration, preferably heated and humidified� �B) Specific:�Surfactant replacement therapy through ET tube.

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Nursing Management:�

• ABGs
• Monitor O2 saturation
• Suctioning (sos)
• Support for family
• Adequate fluids and electrolytes
• Replace surfactant [Curasurf )
• Pass ETT if indicated
• O2 therapy
• Ventilator: helps keep small air sacs prevent from collapsing

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Transient Tachypnea of the Newborn (TTN).

• TTN is a respiratory disease of near-term or term infants who display respiratory distress shortly after delivery.
• It occurs when the infant fails to clear the airway of lung fluid or mucus or has excess fluid in the lungs, this limit the amount of alveolar surface available for gas exchange, leading to respiratory rate and depth to better use of the surface available.

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Risk factors:

· Infant born by Cesarean section, in which the thoracic cavity is not squeezed by the force of vaginal pressure, so that less lung fluid is expelled than normally happen.

Clinical presentation:�* The infant is usually near-term or term.�* Exhibits tachypnea (> 80 breaths/min) shortly after delivery. �* The infant may also display mild grunting, nasal flaring, intercostals retraction, and cyanosis.�* Spontaneous improvement of the neonate, which considered as the most important marker of TTN.�

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Management of TTN:�- Oxygenation.�- Fluid restriction.�- Start feeding as tachypnea improves.�Outcome and prognosis:�·Peaks intensity reached at 36 hours of infant’s life.�·The disease is self-limited (respiratory symptoms improve as intrapulmonary fluid is naturally absorbed or artificially mobilized using diuresis).�·No risk of recurrence or further pulmonary dysfunction.

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C) Meconium Aspiration Syndrome (MAS).�Definition: � This respiratory disorder is caused by meconium aspiration by the fetus in utero or by the newborn during labor and delivery. MAS is often a sign that the neonate has suffered asphyxia before or during birth. The mortality rate can be as high as 50% and survivors may suffer long-term sequelae related to neurological damage. �

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Causes and Pathophysiology:�1. Fetalis hypoxia; e.g. cord prolapse that comes around the neck of the fetus many days before delivery. �2. Babies born breech presentation.�In both cases; intrauterine hypoxia Or breech presentation vagal nerve stimulation relaxation of the sphincter muscle �releasing of the first stool (meconium) in the intrauterine life and becomes mixed with the amniotic fluid, with the first breath the baby can inhale meconium.

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Dangerous of MAS:�The aspirated meconium can cause airway obstruction clinical manifestations of RDS, and an intense inflammatory reaction.

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PPHN

• Persistent pulmonary hypertension of the newborn (PPHN) is defined as the failure of the normal circulatory transition that occurs after birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left intracardiac shunting of blood.

Sign and symptoms

• Asphyxia
• Tachypnea, respiratory distress
• tricuspid regurgitation
• Low Apgar scores
• Cyanosis; poor cardiac function and perfusion
• Systemic hypotension
• Symptoms of shock

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PPHN nursing management

• Continuous monitoring of oxygenation, blood pressure, and perfusion
• Maintaining a normal body temperature
• Correction of electrolytes/glucose abnormalities and metabolic acidosis
• Nutritional support
• Minimal stimulation/handling of the newborn
• Minimal use of invasive procedures (eg, suctioning)
• Pulmonary vasodilators
• Prostaglandine

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Hyperbilirubinemia

• Definition:�Hyperbilirubinemia is an elevation in the neonatal serum bilirubin characterized by JAUNDICE, which is defined as “yellowish discoloration of skin and mucous membranes”. In the neonate clinical jaundice is diagnosed if the total serum bilirubin is ≥ 7 mg/dl.
• N.B.: � The normal adult range of Total Serum Bilirubin is 0.2 – 1 mg/dl (Direct: 0 – 0.2 mg/dl and Indirect: 0.2 – 0.8 mg/dl).

Pathophysiology: = Neonatal Bile Pigment Metabolism.�Destruction of RBCs� � �Hemoglobin Salts Water� �Heme globin� (protein portion reused by the body).� + O2� �Biliverdin�

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+�more O2� �Unconjugated Bilirubin�+�Plasma protein� � �Liver�Which released from plasma protein inside the liver and connected with Glucuronic acid and Glucuronyl Transferese Enzyme (in the presence of normal Ph, O2, and normal body temperature) to become Conjugated Bilirubin, that has 3 pathways:� �Bile duct Kidney Gastrointestinal tract�To digest fat. (Urobilin Urobilinogen) (Stercobilin Stercobilinogen) � to obtain normal color of urine. to obtain normal color of stool.

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The following are possible causes of hyperbilirubinemia in the newly born infants:�1. Over production of bilirubin.�2. Under excretion of bilirubin.�3. Combined over production and under excretion.�4. Physiological jaundice.�5. Breast milk associated jaundice.

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Complication:� The most common complication of hyperbilirubinemia is Kernicterus (Bilirubin Encephalopathy), which usually occurs when the unconjugated serum bilirubin level exceeds than 20 mg/dl. In small, sick preterm infants, even a bilirubin level in a low range may cause Kernicterus.(17 mg/dl)

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Management of unconjugated hyperbilirubinemia

• Prophylactic treatment:�Phenobarbitone
• Blood exchange transfusion �Carry out this technique Beside the Crash Cart.
• Phototherapy:�Nursing care for those infants receiving Phototherapy:�1.     Cover the infant’s eyes and genital organs.�2.     The infant must be turned frequently to expose all body surface areas to the light.�3.     Serum bilirubin level /4 – 12-24 hours.�4.     Each shift, eyes are checked for evidence of discharge or excessive pressure on the lids and eye care should be done using warm water, then apply eye drops or ointment.

5. Eye cover should be removed during feeding, and this opportunity is taken to provide visual and sensory stimuli.�6. Avoid oily lubricants or lotion on the infant’s exposed skin, because this can act as a barrier that prevent penetration of light through the skin.�7. Increase feeds in volume and calories. Add 20% additional fluid volume to compensate for insensible and intestinal water loss. �8. Intake and output chart. �

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HYPOGLYCEMIA

• Definition:�Neonatal hypoglycemia is usually defined as a serum glucose value of < 40-45 mg/dl. is considered abnormal (hypoglycemia).
• Untreated hypoglycemia can result in permanent neurological damage or death.
• �N.B.: The normal plasma glucose concentration in the neonate is approximately 70 – 80 mg/dl in neonates of normoglycemic mothers.

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*) Neonates at risk for developing hypoglycemia:�1- The main cause may become maternal malnutrition during pregnancy which leads to fetal malnutrition and of course a low birth weight.��2- Those infants whom are Small for gestational age infants (SGA), that manifested by decrease in their birth weight and subcutaneous fat and hepatic glycogen.� �3- Those infants’ of diabetic mothers (IDM) or those named as large for gestational age (LGA).

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4- Those whom placentas were abnormal,�e. g.: placenta previa.�5- Those whom their mothers had toxemia during pregnancy, e. g.: eclampsia or pre-eclampsia induction of labor preterm infant.�6- Those very ill or stressed neonates whom their metabolic needs were increased due to hypothermia, infection, respiratory distress syndrome, or cardiac failure.�

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Pathophysiology:� The fetus receives glucose from the mother continuously across the placenta. As soon as the cord is cut, within 2 hours the normal neonate’s blood glucose level falls from 70 – 80 mg/dl to 50 mg/dl. At this time, hepatic glucose is released into the blood and the serum glucose level returns to its normal level at birth (70 – 80 mg/dl). So, after birth the neonate must kept well nourished because of the newly acquired stressors as; abrupt transition from warm intrauterine environment to a relatively cold extra-uterine one, beginning the respiratory cycles by the neonate own self, muscular activity, and suckling effort to prevent carbohydrates storage consumption and the neonate become at risk for developing hypoglycemia.�

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Clinical manifestations:�1-    Hypotonia.�2-    Feeding poorly after feeding well.�3-    Tremors.�4-    Cyanotic spells.�5-    Lethargy.�6-    Seizures.�

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7-    Hypothermia.�8-    Irregular respiratory pattern (Apnea).�9-    Irritability.�10- High pitched cry followed by weak cry.�11- poor reflexes, especially sucking reflex.

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Management of the Neonate at Risk:�Prevention:�providing a warm environment. � Early enteral feeding is the single most important preventive measure.�If enteral feeding is to be started, breast or artificial milk should be used if the infant is able to tolerate nipple or naso-gastric tube feeding.

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These infants should have glucose values monitored until they are taking full feedings and have three normal pre-feeding readings above 40-45 mg/dl. Care must be taken to ensure that breast-feeding mothers are providing an adequate intake. �If the infant at risk for hypoglycemia is unable to tolerate nipple or tube feeding, maintenance IV therapy with 10% glucose should be initiated and glucose levels monitored.

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Management of the Neonate with Hypoglycemia:��Infants who develop hypoglycemia should immediately be given 2cc/kg of 10% dextrose over 5 minutes, repeated as needed. �

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A continuous infusion of 10% glucose at a rate of 8-10 mg/kg/min should be started to keep glucose values normal (NOTE: 10 mg/kg/min of 10%dextrose = 144cc/kg/day). Frequent bedside glucose monitoring is necessary.�When feedings are tolerated and frequent bedside glucose monitoring values are normal, the infusion can be tapered gradually.

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Neonatal Sepsis�

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Introduction:� The newborn infant is uniquely susceptible to acquire infection, whether bacterial, viral or fungal. Bacterial sepsis and meningitis continue to be major causes of morbidity and mortality in the newborn. The mortality rate due to sepsis ranges from 20% to as high as 80% among neonates. Surviving infants can have significant neurologic weakness because of CNS involvement.

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Definition:� Neonatal sepsis is a disease of neonates (who are younger than one month) in which they are clinically ill and have a positive blood culture.�

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Risk Factors:�I) Maternal risk factors:�- e.g.: Premature rupture of membrane.�II) Neonatal risk factors:�- e.g.: Prematurity (less immunologic ability to resist infection + more liable to penetrate their defensive barriers).�

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Bacteria can reach the fetus or newborn and cause infection in one of the following ways:

• Bacteria can pass through the maternal blood through placenta .
• Bacteria from the vagina or cervix can enter the uterus, as groups B streptococci.
• The newborn may be come contract with bacteria as it passes through the birth canal as gram negative organisms.
• The newborn may come in contact with bacteria in its environment after birth

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Clinical presentation of neonatal sepsis: �Physical findings may be nonspecific. � e.g.: apnea , Jaundice , Hypothermia , Bulging or full fontanel , Seizures , hypotonia

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Laboratory indicators of sepsis include: �- Total leukocytic count (WBC count) �- C – reactive Protein (CRP) �- Erythrocyte Sedimentation Rate (ESR) �- Cultures:�

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Management of Sepsis:�- Prevention: through proper application to infection control practices.�- Early onset sepsis; give intrapartum antimicrobial prophylaxis (IAP) to the mother. �

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- Neonates with clinically suspected sepsis:�*) Culture should be obtained first.�*) The recommended antibiotics are ampicilin and gentamicin.�*) Third generation cephalosporins (Cefotaxime) may replace gentamicin if meningitis is clinically suspected or if gram-negative rods are dominant in the unit.�- Late onset neonatal sepsis: �Vancomycin in combination with either gentamicin or cephalosporins should be considered in penicillin resistant cases.�Note: Administer all medications IV.�

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Nursing consideration

• Prevention

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• Curative

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Prevention

1- Demonstrate the effect of hand washing upon the prevention of the noscomical infections.

2 -Standard precautions should be applied in the nursery for infection prevention.

3- Instillation of antibiotics into newborn’s eye 1-2 hours after birth is done to prevent the infection.

4- Skin car should be done using worm water and may use mild soup for removal of blood or meconium and avoid the removal of vernix caseosa.

5- Cord care should be cared out regularly using alcohol or an antimicrobial agent.

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�Curative �

• Encourage breast feeding from the mother.
• Adequate fluid and caloric intake should be administered by gavage feeding or intravenous fluid as ordered.
• Extra-measure for hypothermia or hyperthermia that may take place to the newborn.
• Administering medications as doctor order.
• Follow the isolation precautions.
• Monitoring intravenous infusion rate and antibiotics are the nurse responsibility.

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• Administer the medication in the prescribed dose, route, and time within hour after it is prepared to avoid the loss of drug stability.
• Care must be taken in suctioning secretions from the newborn as it may be infected.
• . Isolation procedures are implemented according to the isolation protocols of the hospital.
• Observe for the complication e.g. meningitis and septic shock.
• Encourage in-service programs and continuing education of nurses regarding the infection control precautions.

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�Birth Asphyxia �

• failure to initiate and sustain breathing at birth
• Incidence 3-5%
• Hypoxia,hypoperfusion,hypercapnia,acidosis
• Multiorgan dysfunction-HIE�Risk factors-poor predictors

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Risk factors

• GDM
• HTN
• DM
• Prolong labor
• Age <16 or >35
• Pre mature or post term
• GA
• Abnormal presentation
• Congenital abnormality

Symptoms of Birth Asphyxia

• Symptoms of asphyxia in a baby at the time of birth may include:
• Baby is not breathing or breathing is very weak
• Skin color is bluish or pale
• Heart rate is low
• Muscle tone is poor or reflexes are weak
• Too much acid is in the blood (acidosis)
• The amniotic fluid is stained with meconium
• The baby is experiencing seizures

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Treatment may include:

• Giving the mother extra oxygen before delivery
• Emergency delivery or Caesarean section
• Assisted ventilation and medications to support the baby's breathing and blood pressure
• Oxygen inhalation
• Suctioning
• CPR
• Extracorporeal membrane oxygenation (ECMO)

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G6PD

• G6PD Deficiency is a hereditary abnormality in the activity of an erythrocyte (red blood cell) enzyme. This enzyme, glucose-6-phosphate dehydrogenase (G-6-PD), is essential for assuring a normal life span for red blood cells, and for oxidizing processes. This enzyme deficiency may provoke the sudden destruction of red blood cells and lead to hemolytic anemia with jaundice 

Sign and symptoms

• Sudden rise of body temperature and yellow coloring of skin and mucous membrane.
• Dark yellow-orange urine.
• Pallor, fatigue, general deterioration of physical conditions.
• Heavy, fast breathing.
• Weak, rapid pulse.

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Inborn errors of metabolism

• Inborn errors of metabolism are rare genetic disorders in which the body cannot properly turn food into energy. The disorders are usually caused by defects in specific proteins (enzymes) that help break down (metabolize) parts of food.
• A food product that is not broken down into energy can build up in the body and cause a wide array of symptoms. Several inborn errors of metabolism cause developmental delay if not controlled.

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• A few examples are:
• Fructose intolerance�Galactosemia�Maple sugar urine disease (MSUD)�Phenylketonuria (PKU)

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Nursing Care of the Newborn � with Inborn Errors of Metabolism

• Assessment of signs of the disorder
• State-mandated newborn testing
• Referral of parents to support groups
• Referral of parents to centers for education
• Dietary management

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