Birth injuries and icterus neonatarum

DEEPTHY P. THOMAS

II YEAR MSc NURSING

GOVT.COLLEGE OF NURSING

ALAPPUZHA

BIRTH INJURIES AND ICTERUS

NEONATARUM

DEFINITION-birth injuries

An impairment of the infant’s body function or structure due to adverse influences that occurred at birth.

National Vital Statistics Report

Birth injuries is defined as those sustained during labour and delivery. Birth injuries may be severe enough to cause neonatal deaths, still births or number of morbidities.

D C Dutta

RISK FACTORS

Primiparity

Small maternal stature

Maternal pelvic anomalies

Prolonged or unusually rapid labor

Oligohydraminos

Malpresentation of the fetus

Use of mid forceps or vacuum extraction

Versions and extraction

Very low birth weight or extreme

prematurity

Fetal macrosomia or large fetal head

Fetal anomalies

PREDISPOSING FACTORS

Prolonged or obstructed labor

Fetal macrosomia

Cephalopelvic disposition

Abnormal presentation (breech)

Instrumental delivery

Difficult labor

Shoulder dystocia

Precipitate labor

TYPES OF BIRTH INJURIES

Soft tissue: skin- laceration, abrasions,

aft necrosis.

Nerve: facial nerve, brachial plexus,

spinal cord, phrenic nerve, horner’s

syndrome

Eye: hemorrhages-subconjunctiva,

retina

Viscera: rupture of liver, adrenal gland,

spleen

Scalp: laceration, abscess,

haemorrhage.

Dislocation: hip, shoulder, cervical

vertebrae

Skull: cephal hematoma, subgleal

hematoma, fractures

Intracranial: haemorrhages-

intraventricular, subdural, subarachanoid

Bones: fractures-clavicle, humerus,

femur

HEAD AND NECK INJURIES

1.injuries associated with intrapartumfetal monitoring

2. Extracranial hemorrhage

b) cephalohematoma

b) cephalohematoma

c) subgleal hematoma

3. Intracranial haemorrhage

4. Skull fracture

5. Facial or mandibular fractures

6. Nasal injuries

7. ocular injuries

8. Ear injuries

9. Sternocleidomastoid injury

10. Pharyngeal injury

caput succedaneum:

it is a commonly occurring subcutaneous,

extraperiosteal fluid collection that is

occasionally hemorrhagic.

It has poorly defined margins and can extend

over the midline and across suture lines.

The lesion usually resolves spontaneously

without sequeale over the first several days

after birth.

Vacuum caput is a caput succedaneum with

margins well demarcated by the vacuum cup.

cephalohematoma

It is a collection of blood between the

pericranium and flat bone of the skull,

usually unilateral and over the parietal

bone.

Causes

rupture of small emissary vein from the

skull and may be associated with

fracture of the skull bone. It is never

present at birth but gradually develops

after 12-24 hours.

The condition may be confused with

caput succedaneum or meningocele.

Meningocele always lies over a suture

line or over a fontanelle and there is

impulse on crying. Prognosis is good.

subgleal hematoma

subgleal hematoma is hemorrhage

under the aponeurosis of the scalp. It is

more often seen after vaccum or forceps

assisted deliveries.

the hemorrhage can spread across the

entire calvarium.

Intracranial haemorrhageTraumatic:

Extradural haemorrhage:

Subdural:

Slight haemorrhage may occur following:

A] fracture of skullbone

B] rupture of the inferior sagital sinus

C] rupture of small veins leaving the cortex

massive haemorrhage:

a] tear of the tendorium cerebrii

b] injury of superior sagital sinus

mechanism of tentorial tear:

normally falx cerebri attached to the tentorium

cerebri and both anchoring the base of the skull

to the vault.

This results in the upward movement of the

vault from the base.

As a result, too much strain is put on the vertical

fibres of tentorium cerebella- called stress

fibres.

If the moulding is excessive or applied suddenly,

these fibres are torn.

as a result it allows excessive elongation of the

vault until the tear extends to involve the

straight sinus or vein of Galen or its tributaries.

Causes

excessive moulding in deflexed vertex with

gross disproportion.

Rapid compression of the head during the

delivery of after coming head of breech or in

precipitate labor.

Forcible forceps traction following wrong

application of the blades.

Clinical features

The hemorrhage may be fatal

the baby is delivered stillborn or with severe

respiratory depression having an apgar score

0-3.

The features cerebral irritation include

frequent high pitch cry, neck retraction, in-

coordinate ocular movements, convulsions,

vomiting and bulging of anterior fontanelle.

Anoxic:

Intraventricular

Subarachanoid.

Intracerebral.

PREVENTION

To prevent or to detect earliest, intrauterine

fetal asphyxia

To avoid traumatic vaginal delivery.

To extend the use of caesarean section in

breech more liberally.

Administration of vitamin K 1 mg

intramuscularly soon after birth

INVESTIGATIONS:

Ultrasongraphy used to detect intraventricular

hemorrhage

Doppler ultrasonography to detect any change

in the cerebral circulation.

CT scan is useful to detect cortical neuronal

injury.

MRI used to identify hypoxic ischemic brain

injury.

CSF: hemorrahage

TREATMENT

The baby should be nursed in quite

surroundings.

Incubator nursery is preferable to supply

oxygen and to maintain the temperature and

humidity.

To maintain cleanliness of the air passages.

To maintain normal range of PaCO2 and to

avoid hypoxemia

To restrict handling the baby, as such bathing,

weighing and measuring should be withheld.

Feeding by nasogastric tube is advisable.

Fluid balance is to be maintained, if necessary

by parenteral route.

To administer vitamin K 1 mg intramuscularly

to prevent further bleeding due to

hypoprothrobinemia.

Prophylactic antibiotics is to be administered.

Anticonvulsants: phenobarbitone 5-10

mg/kg/day in divide doses at 6 hourly intervals

intramuscularly, phenytoin 10-15 mg/kg/day

with cardiac monitoring

Subdural tap for subdural hematoma

Skull fracture

Fracture of the vault of the skull may be

fissure or depressed type.

Fractures are due to

Effect of difficult forceps in disproportion or

due to wrong application of the fo4rceps.

Projected sacral promontory of the flat

pelvis may produce depressed fracture

even though the delivery is spontaneous.

Facial or mandibular fractures

Facial fractures can be caused by numerous

forces, including natural passage through the

birth canal, forceps use or delivery of the head

in breech presentation.

Nasal injuries

Nasal fracture and dislocation may occur

during the birth process. The most frequent

nasal injury is dislocation of the nasal

cartilage, which may result from pressure

applied by the maternal symphysis pubis or

sacral promontory.

ocular injuries

They result from increased venous congestion

and pressure during delivery. Retinal

hemorrhages usually resolve within 1 to 5

days. Sub-conjunctival hemorrhages reabsorb

within 1 to 2 weeks.

Ear injuries

Ears are susceptible to injury particularly

with forceps application. More significant

injuries occurs with fetal malposition.

Sternocleidomastoid injury

referred to as congenital or muscular

torticollis. The etiology is uncertain. The most

likely cause is a muscular compartment

syndrome resulting from intrauterine

positioning.

Pharyngeal injury

Minor submucosal pharyngeal injuries

can occur with postpartum bulb

suctioning. More serious injury, such as

perforation into the mediastinal or

pleural cavity, may result from

nasogastric or endotracheal tube

placement.

CRANIAL NERVE, SPINAL CORD

AND PERIPHERAL NERVE INJURY

Cranial nerve injury

Facial nerve injury:

Recurrent laryngeal injury

spinal cord injuries

Vaginal delivery of an infant with a hyper

extended neck or head, breech delivery and

severe shoulder dystocia are risk factors for

spinal cord injury. Injuries include spinal

epidural hematomas, vertebral artery

injuries, traumatic cervical hematomyelia,

spinal artery occlusion and transaction of

the cord.

cervical nerve root injury

Phrenic nerve injury

Phrenic nerve damage leading to

paralysis of ipsilateral diaphragm may result

from a stretch injury due to lateral hyper

extension of the neck at birth. Risk factors

include breech and difficult forceps deliveries.

Brachial plexus injury

The cause is excessive traction on the head,

neck and arm during birth.the risk factors

include shoulder dystocia, macrosomia,

malpresentation and instrumented deliveries.

Duchenne- Erb palsy involves the upper

trunks (C5, C6 and occasionally C7) and is

the most common type of brachial plexus

injury. The arm is typically adducted and

internally rotated at the shoulder. There is

extension and pronation at the elbow and

flexion of the wrist and fingers in the

characteristics “waiter’s tip” posture, the

deltoid, infraspinatus and biceps, supination

and brachioradialis muscles and the

extensors of the wrist and the fingers may be

weak or paralysed. The moro, biceps, and the

radial reflexes are absent on the affected side.

Diaphragm paralysi occurs in 5% of cases.

Total brachial plexus injury accounts for

approximately10% of all cases. The entire

arm is flaccid. All reflexes including grasp and

sensation, are absent. If sympathetic fibres

are injured at T1, Horner syndrome may be

seen.

Klumpke palsy rarest of the palsies

accounting for <1% of brachial plexus

injuries. The lower arm paralysis affects

the intrinsic muscles of the hand and the

long flexors of the wrist and fingers. The

grasp reflex is absent. However, the

biceps and radial reflexes are present.

There is sensory impairment on the

ulnar side of the forearm and the hand.

Because the first thoracic root is actually

injured, its sympathetic fibres are

damaged, leading to an ipsilateral

Horner syndrome.

BONE INJURIES

clavicular fracture

These fractures are seen in vertex

presentations with shoulder dystocia

or in breech deliveries when the arms

are extended

long bone injuries

Humeral fractures typically occur during

adifficulty delivery of the arms in the breech

presentation and/ or of the shoulder in vertex.

Direct pressure on the humerus may also

result in fracture.

Femoral fractures usually follow a

breech delivery. Infants with congenital

hypotonia are at increased risk. Physical

examination usually reveals an obvious

deformity of the thigh

INTRA ABDOMINAL INJURIES

Hepatic injury

Splenic injury

Adrenal hemorrhage

SOFT TISSUE INJURIES

petechiae and ecchymosesThe birth history, location of lesions, they are

rarely appearance without new lesions, and the

absence of bleeding from other sites help to

differentiate petechiae and ecchymoses

secondary to birth trauma from those caused by a

vasculitis or coagulation disorder.

lacerations and abrasions

It may be secondary to scalp electrodes and

fetal scalp blood sampling or injury during birth.

Deep wound may require sutures. Infection is a

risk particularly with scalp lesions and an

underlying caput succedaneum or hematoma.

Treatment includes cleansing the wound and the

close observation.

Subcutaneous fat necrosis

It is not usually recognized at birth. It

usually presents during the first 2 weeks after

birth as sharply demarcated; irregularly

shaped; firm and non pitting subcutaneous

plaques or nodules on the extremities, face,

trunk or buttocks. The injury may be colorless

or have a deep red or purple discoloration.

Calcification may occur. No treatment is

necessary. Lesions typically resolve

completely over several weeks to months.

PREVENTION OF INJURIES IN

NEWBORN

ANTENATAL PERIOD

To screen out the at risk babies likely to

be traumatized during vaginal delivery and to

employ liberal use of elective CS. Contracted

pelvis and CPD or malpresentation like

breech or transverse lie are included in the list

INTRANATAL PERIOD

Normal delivery

continous fetal monitoring to prevent traumatic

cerebral anoxia

episotomy should be done carefully

the neck should not be unduly strechted while

delivering the shoulder to prevent injuries to the

brachial plexus or sternomastoid.

Special care to the preterm to prevent anoxia,

avoid strong sedatives, liberal episiotomy and to

administer Vit K 1mg IM to prevent haemorrhage

from the traumatized site.

Forceps delivery

Difficult forceps are to be avoided in preference to the safer CS.

Never apply traction unless the application is a correct one.

Ventouse delivery

It is relatively less traumatic. But it should be avoided in preterm.

Vaginal breech delivery

Proper selection of cases and utmost care and gentleness are to be executed while conducting breech delivery. Most crucial period of breech delivery is the delivery of the after coming head.

NURSING ASSESSMENT

Recognition of trauma and birth injuries is imperative so that early treatment can be initiative.

Review the labor and birth history for risk factors, such as a prolonged or abrupt labor, abnormal or difficult presentation, cephalopelvic disproportion or mechanical forces such as forceps or vaccum used during delivery.

Also review the history for multiple fetus deliveries, large for date infants, extreme prematurity, large fetal head or newborns with congenital anomalies.

Complete a careful physical and neurologic assessment of every newborn admitted to the nursery to establish whether injuries exist.

Inspect the head for lumps, bumps or bruises.

Note if swelling or bruising crosses the suture

line.

Assess the eyes and face for facial paralysis,

observing for asymmetry of the face with crying or

appearance of the mouth being drawn to the

unaffected side.

Ensure that the newborn spontaneously moves

all extremities.

Note any absence of or decrease in the deep

tendon reflexes or abnormal positioning of

extremities.

Assess and document symmetry of structure and

function. Be prepared to assist with scheduling

diagnostic studies to confirm trauma or injuries,

which will be important in determining treatment

NURSING MANAGEMENT

Nursing management is primarily supportive

and focuses on assessing for resolution of the

trauma or any associated complications along

with providing support and education to the

parents.

Provide the parents with explanations and

reassurance that these injuries resolve with

minimal or no treatment.

Parents are alarmed when their newborn is

unable to move an extremity or demonstrates

asymmetric facial movements.

Provide parents with a realistic picture of

situation to gain their understanding and trust.

Be readily available to answer questions and

teach them how to care for their newborn,

including any modifications that might be

necessary.

Allow parents adequate time to understand the

implications of the birth trauma or injury and what

treatment modalities are needed, if any.

Provide them with information of length of time

until the injury will resolve and when and if they

need to seek further medical attention for the

condition.

Spending time with parents and providing them

with support, information and teaching are

important to allow them to make decisions and

care for their newborn.

Anticipate the need for community referral for

ongoing follow up and care, if necessary.

ICTERUS

NEONATARUM

ENTERO HEPATIC CIRCULATION

AND NORMAL BILIRUBIN

METABOLISM IN A NEWBORN 1. Source of production: Bilirubin is derived

from the breakdown of hemeproteins which are

present in hemoglobin, myoglobin and certain

heme containing enzymes. Three fourths of the

bilirubin comes from hemoglobin catabolism.

One gram of hemoglobin results in the production

of 34 mg of bilirubin. A normal term newborn

produces about 6-10 mg/kg/ day of bilirubin.

2. Metabolism

i. Bilirubin is bound to albumin for transport in

the blood. This bound bilirubin does not enter

the central nervous system and is nontoxic.

ii. Upon reaching the liver, only bilirubin enters

the liver cell and gets bound to ligandin which

helps to transport it to the site of conjugation.

iii. Conjugation occurs with glucuronic acid to

produce mono- and diglucuronides which are

water soluble.

The conjugated bilirubin is transported with

the bile to the gut. In the sterile newborn gut,

there is an enzyme called beta- glucuronidase

which converts bilirubin glucuronide into

unconjugated bilirubin which is reabsorbed

into the circulation.

DEFINITION OF

HYPERBILIRUBINEMIA

The term Hyperbilirubinemia refers to an excessive level of accumulated bilirubin in the blood and is characterized by Jaundice or Icterus, a yellowish discolouration of the skin, sclera and nails.

Hyperbilirubinemia is caused by excessive concentrations of bilirubin in blood, which can result in Jaundice.

When the bilirubin [unconjugated] level rises more than the arbitrary cut-off point of 10 mg%, the condition is called hyperbilirubinemia of the newborn

CAUSES OF

HYPERBILIRUBINEMIA

Physiological

The jaundice appears on 2nd and 3rd day and

disappears by 7-10th day, a little later in

premature neonates. In term infant the level may

be 6-8 mg /dl on the 3rd day. arise of

unconjugated serum bilirubin to 12 mg/dl in the

first week may be without any abnormality.

Causes of excessive bilirubinproduction are:

Increased red cell volume and increased red cell destruction due to shorter life span in the neonate.

Transient decreased conjugation of bilirubin due to decreased UDPG-T activity

Increased enterohepatic circulation due to decreased gut mobility.

Decreased hepatic circulation due to decreased gut motility.

Decreased hepatic excretion of bilirubin

Decreased liver cell uptake of bilirubin due to decreased ligandin

Pathological:

Excessive red cell hemolysis

Hemolytic disease of the newborn

Neonatal septicemia: specially with e-coli.

Blood extravastion: sequestration of blood

within the cavities can cause increased

bilirubin.

Defective conjugation of bilirubin

Congenital deficiency of glucuronyl

transferase

Crigler najjar syndrome[ autosomal

recessive], gilbert syndrome [autosomal

dominant], preterm babies with impaired

liver function.

Breast milk jaundice:

The enzyme glucuronyl activity of the liver

is inhibited by a specific steroid 3α,20β-

pregnanediol and increased fatty acids of

breast milk. The bilirubin level rises from

the fourth day after birth to a maximum of

Metabolic disorders:

Galactosemia, hypothyroidism may be associated

with unconjugated hyperbilirubinemia

Increased enterohepatic circulation of

unconjugated bilirubin. It is seen with

duodenal atresia, pyloric stenosis.

Substances and disorders that affect binding

of bilirubin to albumin: aspirin, sulphonamides,

fatty acids and asphyxia, acidosis, sepsis or

hypothermia increases free unconjugated bilirubin

level.

Miscellaneous: congenital obstruction, viral

hepatitis, syphilis.

PATHOPHYSIOLOGY

Bilirubin production is increased due to

increased production of erythtocytes.

Heme

Heme oxygenase

biliverdin

Disslove in water

Unconjugated biirubin[insoluble]

Bound to albumin

Transported in plasma

Reaches the liver

Bilirubin transfered to liver cells

Binds with ligandin

Ligandin concentrations are low at birth

UGPT

Bound to glucuronic acid

Conjugated bilirubin

Water soluble molecule

Excreted into bile

Physiologic Jaundice

Increased bilirubin load on the

hepatic cell

Defective uptake from plasma into

liver cell

Defective conjugation

Decreased excretion

Increased entero-hepatic circulation

Characteristics of physiological jaundice.

First appears between 24-72 hours of

age

Maximum intensity seen on 4-5th day in

term and 7th day in preterm neonates

Bilirubin level does not exceed 15 mg/ dl

Clinically undetectable after 14 days.

No treatment is required but baby should

be observed closely for signs of

worsening jaundice.

Pathological jaundice

Clinical jaundice detected before 24

hours of age

Rise in serum bilirubin by more than 5

mg/ dl/ day

Serum bilirubin more than 15 mg/ dl

Clinical jaundice persisting beyond 14

days of life

Clay/white colored stool and/or dark

urine staining the clothes yellow

Direct bilirubin >2 mg/ dl at any time

TYPES OF HYPERBILIRUBINEMIA

Conjugated Hyperbilirubinemia

Unconjugated Hyperbilirubinemia

Conjugated hyperbilirubinemia(direct)

Diseases that reduce the rate of secretion of

conjugated bilirubin into the bile or the flow of bile

into the intestine produce a mixed or

predominantly conjugated hyperbilirubinemia due

to the reflux of conjugates back into the plasma

Causes of conjugated

Hyperbilirubinemia

Infective

Viral

CMV, Rubella, Reovirus III, Hepatitis B

Bacterial

E. Coli, Listeria,

Protozoal

Toxoplasma

Inherited Causes

Galactosemia

Alpa-1 antitrypsin deficiency

Biliary Hypoplasia (Syndromic)

Cholestasis with actin and microfilament

accumulation

Progressive intrahepatic cholestasis

Iron storage disorders

Chromosomal Anomalies:

Trisomy 13

Trisomy 18

Trisomy 21

Idiopathic Causes

Biliary atresia - Neonatal Hepatitis

Choledochal cyst

Circulatory Abnormalities

Hypoxia

Anemia

Miscellaneous Causes:

TPN

Hypothyroidism

Maternal alcohol ingestion

Erythromycin estolate

Frusemide

Hemolytic disease

UNCONJUGATED

HYPERBILIRUBINEMIA

(INDIRECT)

Types:

Physiologic jaundice: It is caused due to

immature hepatic function plus increased bilirubin

load from red blood cell (RBC) hemolysis. Its

onset is after 24 hours (Preterm infants,

prolonged). It becomes peak on 72-90 hours. It

declines on 5th to 7th day.

Treatment:

Increase frequency of feedings and avoid

supplements.

Evaluate stooling pattern.

Monitor Transcutaneous bilirubin (TcB) or Total

Serum Bilirubin level.

Perform risk assessment.

Use Phototherapy, if bilirubin levels increase

significantly or significant hemolysis is present

BREAST FEEDING ASSOCIATED JAUNDICE (EARLY ONSET):

It is due to decreased milk intake related to fewer calories consumed by infant before mother’s milk is well established

It’s onset is from second to fourth day. It’s peak is from 3rd to 5th day and duration is variable.

Treatment:

Breastfeed frequently ( 10- 12 times/ day)

Evaluate stooling pattern

Perform risk assessment.

Use phototherapy if Bilirubin levels increase significantly

Assist Mother with maintaining milk supply; feed expressed milk as appropriate.

After discharge , follow up according to hour of discharge.

BREAST MILK JAUNDICE( LATE ONSET):

It is because of the possible factors in breast milk that prevent bilirubin conjugation and less frequent stooling. It’s onset is fifth to seventh day and peak from tenth to fifteenth day. It’s duration is 3-12 weeks or more.

Treatment:

Increase frequency of breast feeding

Perform risk assessment.

Consider performing additional evaluations

May include home phototherapy with a temporary (10-12 hour)

Assist mother with maintenance of milk supply and therapy.

Use formula supplements only at Practitioner’s discretion.

HEMOLYTIC DISEASE:

It is due to Blood antigen incompatibility causing hemolysis of large number of RBC’S and liver is unable to conjugate andexcrete excess bilirubin from hemolysis. Its onset is during first 24 hours (levels increase greater than 5 mg/day)

Treatment:

Monitor TSB level.

Perform risk assessment.

Postnatal- Use Phototherapy; administer intravenous immunoglobulin per protocol, if severe, perform exchange transfusion.

Prenatal – Perform Fetal Transfusion.

Rh (D) Immunoglobulin.

breast feeding

Minimize maternal – infant separation

CLINICAL FEATURES

yellow color

Drowsiness

neurologic findings, such as changes in muscle

tone, seizures, or altered cry

Hepatosplenomegaly, petechiae, and

microcephaly may be associated with hemolytic

anemia, sepsis, and congenital infections

DIAGNOSTIC MEASURES

Clinical:

Laboratory studies:

Serum bilirubin level > 12 mg/dl,requires further investigations.

Total conjugated bilirubin and unconjugated bilirubin.

Complte hemogram including recticulocyte count

Hemolytic anemia: Hb decreases, recticulocyte count decreases, presence of nucleated red cells.

Polycytemia: hematocrit>65%

Sepsis: WBC count [ total or differential increases.

Hereditary spherocytosis: peripheral blood film

Blood group[ABO,Rh] status: mother and infant for ABO and Rh incompatibility.

Direct coomb’s test: for isoimmunization disorder.

Serum albumin to detect total bilirubin binding sites and to assess the need of albumin infusion.

Other laboratory investigations:

Urine for reducing substance, culture for infection

Hemoglobin electrophoresis

Osmotic fragility test

Thyroid and LFT.

Radiology and ultrasonography to detect intestinal obstruction

THERAPEUTIC MANAGEMENT:

Goals of Treatment:

To prevent Bilirubin encephalopathy and as in

any Blood group incompatibility

To reverse the hemolytic process.

PHOTO THERAPY

Phototherapy is the process of using special light toeliminate bilirubin in the blood.

Indications for Phototherapy

immaturity, acidosis, asphyxia, higher free bilirubin levels

Assessment should be Before Phototherapy:

GA Of the baby

Weight The baby

Postnatal Age

Types of Jaundice

the level of jaundice

American Academy of Pediatrics guidelines

For term healthy babies, can be followed.

2. Guidelines are provided for very low birth

weight babies. As a rough guide, Phototherapy is

indicated at a level equal to 1% of the body

weight (for e.g. 10 mg/dl in a 1000 gm baby or 15

mg/dl in a 1500 gm baby). Exchange blood

transfusion is warranted when the TSB level is 5

mg/dl higher than the phototherapy level.

However, the overall clinical situation needs to be

considered to arrive at a proper decision.

3.In case of hemolysis, start phototherapy at a

lower level.

4. Acidosis, asphyxia, hypoglycemia or sepsis

make the blood brain barrier more porous to

bilirubin. So, consider to start early phototherapy.

5. In case of prolonged jaundice (>3 wk), one

should always check fractional bilirubin

estimation. Phototherapy is contraindicated in the

presence of conjugated hyperbilirubinemia (

2mg/dl) because it may result in Bronze Baby

Syndrome.

Mechanisms in phototherapy

Phototherapy is effective because 3 reactions can

occur when bilirubin is exposed to light, as

follows:

photooxidation

Configurational isomerization

Structural isomerization

The photoisomers of bilirubin are excreted in bile

and, to some extent, in urine

Basic principles regarding

phototherapy:

Wavelength

a dose-response relationship

energy delivered to the infant's skin

the efficiency of phototherapy

the nature and character of the light source

Advantages:

Low risk of overheating the infant

No need for eye shields

Ability to deliver phototherapy with the infant in a

bassinet next to the mother's bed

Simple deployment for home phototherapy

The possibility of irradiating a large surface area

when combined with conventional overhead

phototherapy units (double/triple phototherapy)

Types of phototherapy:

Single surface phototherapy

Double surface photo therapy

Tips towards delivering safe and

effective phototherapy

1. Protect the eyes with eye patches

2. Keep the baby naked with a small nappy to

cover the genitalia

3. After switching on the unit check that all

tubes/bulbs are on

4. Place the baby as close to the lights

Encourage frequent breastfeeding. Unless there is

evidence of dehydration, supplementing

breastfeeding or providing IV fluids is unnecessary.

. Keep diaper area dry and clean

Phototherapy does not have to be continuous and

can be interrupted for feeding, clinical procedures,

and to allow maternal bonding.

Monitor temperature every 4 hours and weight every

24 hours.

Measure plasma/ serum bilirubin frequently ~ every

12 hours. Visual assessment of jaundice during

phototherapy is unreliable

EXCHANGE TRANSFUSION

The procedure involves slowly removing the

patient's blood and replacing it with fresh donor

blood or plasma.

The patient’s blood is slowly withdrawn (usually

about 5 to 20 mL at a time, depending on the

patient’s size and the severity of illness). An equal

amount of fresh, prewarmed blood or plasma

flows into the patient's body. This cycle is

repeated until the correct volume of blood has

been replaced.

Indications:

Neonatal polycythemia (dangerously high red

blood cell count in a newborn)

Rh-induced hemolytic disease of the newborn

Severe disturbances in body chemistry

Severe newborn jaundice that does not respond

to phototherapy with bili lights

Severe sickle cell crisis

Toxic effects of certain drugs.

Indications for exchange transfusion in Rh Isoimmunization.

An exchange transfusion soon after birth is indicated if:

Cord bilirubin is 5mg/dl

Cord Hb is £10 mg/dl, PCV <30

Previous sibling history and positive DCT.

Subsequent exchange transfusions are indicated if:

1. Bilirubin 10 mg/dl within 24 hours of age

2. Bilirubin15 mg/dl between 25-48 hours of age

3. Bilirubin 20 mg/dl after 48 hours of age.

4. Rate of rise of bilirubin is 0.5 mg/dl/hr.

Risks

Blood clots

Changes in blood chemistry (high or low

potassium, low calcium, low glucose, change in

acid-base balance in the blood)

Heart and lung problems

Infection (very low risk due to careful screening of

blood)

Shock if not enough blood is replaced

MAISEL'S CHART

It is used for taking decision regarding

treatment in cases of pathological jaundice. In

presence of any of the following, treat as in

next higher bilirubin category.

Perinatal asphyxia

Respiratory distress

Metabolic acidosis

Hypothermia

Low serum protein

Birth weight <1500 g

Signs of clinical or CNS deterioration

PHARMACOLOGIC

MANAGEMENT

Phenobarbital Therapy

Intravenous Immunoglobulins -0.5 to1 gm/kg

Pharmacologic Therapy:

Zinc/Metalloporphyrin

Ursodeoxycholic acid

COMPLICATIONSAcute bilirubin encephalopathy may include the

following neurologic symptoms:

Extra pyramidal movement disorders

Gaze abnormalities

Lethargy

Auditory disturbances (sensorineural hearing loss)

Hypo or hypertonia, truncal arching

Seizures

Coma

Death

Kernicterus (chronic bilirubin encephalopathy)

may include the following symptoms:

Severe cerebral palsy

Auditory dysfunction

Dental enamel dysplasia

Paralysis of upward gaze

PREVENTION

Pregnancy, labour and delivery

Test all pregnant women for ABO, Rh (D) blood types and red cell antibodies,1,2 during

pregnancy

If the mother has red blood cell antibodies noted antenatally then send cord blood

If the mother has not had antenatal blood tests send:

maternal blood for blood group (ABO/Rh) AND

baby’s cord blood for blood group ,Rh type and DAT

Umbilical cord blood total serum bilirubin, haemoglobin or haematocrit measurements do not aid in the prediction of severe hyperbilirubinaemia

Breastfeeding

Encourage all mothers to breastfeed their babies

8 - 12 times a day in the first 2 - 3 days of life.

Encourage the ingestion of colostrum to increase

stooling which prevents reabsorption of bilirubin.

Supplementation with water does not affect

bilirubin levels and is not recommended. If

supplementation is necessary due to inadequate

intake then give expressed breast milk and/or

formula

Educate parents regarding signs of adequate

hydration, feeding and signs of jaundice

NURSING MANAGEMENT

Assessment of jaundice

Colour

Hydration

Other illness

Feeding

NURSING DIAGNOSIS

Deficient Fluid Volume related to inadequate fluid

intake, photo-therapy, and diarrhea.

Hyperthermia related to the effects of

phototherapy

Impaired skin integrity related to

hyperbilirubinemia and diarrhea

Anxiety related to medical therapy given to the

baby.

Follow up

Babies discharged before 48 hours may need 2

follow up visits, the first visit between 24 - 72

hours and a second between 72 - 120 hours.

Follow up assessment must include:

• baby’s weight and percentage change from birth

weight

• adequacy of intake

• voiding and stooling pattern

• presence or absence of jaundice

• clinical judgement to determine the need for total

serum bilirubin level measurement

THANK YOU…