More coursework: 1 - A | B | C | D | E | F | G | H | I - J | K - L | M | N - O | P - S | T | U - Y





1. All babies below 2100g

2. All babies below 35 weeks.

3. All babies with significant, or persisting, respiratory symptoms.

4. Babies with bilirubin levels likely to require exchange transfusion, or known haemo disease with rapidly rising bilirubin levels despite phototherapy.

5. Babies with symptomatic hypoglycaemia, or asymptomatic but needing tube feeds.

6. Any baby needing to start on antibiotics. Antibiotics may be continued on the postnatal ward later if the baby is well.

7. Any baby in whom there is an expected, or a strong family history of inborn errors of metabolism likely to present in the neonatal period, unless they can be safely monitored and investigated on the wards.

8. Babies requiring tube feeds for any reason.

NB: Babies with Down Syndrome and unilateral Cleft Lip/Palate do not need routine admission. Observe on ward and admit only if feed poorly.

9. Major congenital abnormality likely to require treatment or resulting in illness

10. Babies of opiate or cocaine addicts.

If in doubt, discuss with a senior Paediatrician.

NOTE Babies of diabetic Mums if well at birth and not directly to Neonatal Unit.


Definitions of Neonatal Care

Level 1 Intensive Care (Maximal Intensive Care)

Care given in an intensive care nursery which provides continuous skilled supervision by qualified and specially trained nursing and medical staff. Such care includes support of the infant’s parents.

Level 2 Intensive Care (High Dependency Intensive Care)

Care given in an intensive or special care nursery which provides continuous skilled supervision by qualified and specially trained nursing staff that may care for more babies than in Level 1 Intensive Care. Medical supervision is not so immediate as in Level 1 Intensive Care. Care includes support of the infant’s parents.

Special Care

Care given in a special care nursery, transitional care ward or postnatal ward which provides care and treatment exceeding normal routine care. Some aspects of special care can be undertaken by a mother supervised by qualified nursing staff. Special nursing care includes support and education of the infant’s parents.

Normal Care

Care given by the mother, or mother substitute, with medical or neonatal nursing advice is needed.

Clinical Categories of Neonatal Care

Level I Intensive Care (Maximal Intensive Care)

Level 1 Intensive Care should be provided for babies:

1 Receiving assisted ventilation (including intermittent positive airway pressure, intermittent mandatory ventilation and constant positive airway pressure), and in the first 24 hours after its withdrawal. -

2 Of less than 27 weeks’ gestation for the first 48 hours after birth.

3 With birth weight. of less than 1000 grams for the first 48 hours after birth.

4 Who require major emergency surgery for the pre-operative period and post-operatively for 48 hours.

5 On the day of death.

6 Being transported by a team including medical and nursing staff.

7 Who are receiving peritoneal dialysis.

8 Who require exchange transfusions complicated by other disease processes.

9 With severe respiratory disease in the first 48 hours of life requiring an Fi02 of> 0.6.

10 With recurrent apnoea needing frequent intervention, eg over 5 stimulations in 8 hours or resuscitation with IPPV 2 or more times in 24 hours.

11 With significant requirements for circulatory support, eg inotropes, 3 or more infusions of colloid in 24 hours, or infusions of prostaglandins.

Level 2 Intensive Care (High Dependency Intensive Care)

Level 2 intensive care should be provided for babies

1 Requiring total parenteral nutrition.

2 Who are having convulsions.

3 Being transported by a trained skilled neonatal nurse alone.

4 With arterial line or chest drain.

5 With respiratory disease in the first 48 hours of life requiring an Fi02 of

0.4 - 06.

— 6 With recurrent apnoea requiring stimulation up to five times in an eight hour period or any resuscitation with IPPV

7 Who require an exchange transfusion alone.

8 Who are more than 48 hours post-operative and require complex nursing procedures.

9 With tracheotomy for the first 2 weeks.

Special Care

Special Care should be provided for babies

1 Requiring continuous monitoring of respiration of heart rate, or by transcutaneous transducers.

2 Receiving additional oxygen.

3 With tracheotomy after the first 2 weeks.

4 Being given intravenous glucose and electrolyte solutions.

5 Who are being tube fed.

6 Who have had minor surgery in the previous 24 hours.

7 Who require terminal care but not on the day of death.

8 Being barrier nursed.

9 Undergoing phototherapy.

10 Receiving special monitoring (for example frequent glucose or bilirubin estimations).

11 Needing constant supervision (for example babies whose mothers are drug addicts).

12 Being treated with antibiotics.

Resources Required for Neonatal Care


-the BPA recommendation and the Neonatal Nurses Association guidelines for staffing are- as follows, but are subject to local conditions and are not, as yet, founded on research on dependency levels. On presentation of appropriate research findings, these may require amending.


Trained Nurses hold RGN, RM, RSCN or EN. Qualified Nurses hold a certificate in Intensive Care of the Newborn, eg English National Board Course 40& 409, 904, 904Acertificate or Joint Board of Clinical Studies certificate, ie 400, 401, 402.

Maximal Intensive care (Level 1 Intensive Care)

5.5 nurses (wte) qualified and trained per cot.

High Depen&ncy Intensive Care (Level 2 Intensive Care)

3.5 nurses wte qualified and trained per cot.


ProblemsPhysiological and/or anatomical, related to

a H.M.D. — Lack of surface active materials, lung — Type II

alveoli cells immature (Type I line alveoli) therefore do

not reproduce sufficient amounts. Surfactant reduces

surface tension, keeps alveoli open.

b) Apnoea and intermittent respirations

Immature respiratory centre thought to be cause of intermittent respirations.

Apnoea can be induced through changes in physical or environmental conditions eg., Infections, Hyperthermia or Hypothermia (metabolizing brown fat uses 02 leading to anoxia)

2 Hypothermia

a) Less subcutaneous fat.

b) Decreased muscle activity.

c) Reduced oxygen consumption.

d) Less brown fat - produces heat.

3 Jaundice

a) Immature liver enzyme activity.

b)Excess bilirubin production - high foetal Hb

- Cephalohaematoma

- Intra—uterine infections

4 Infections

a) Low 1 gM and 1 gA (1 gM particular response to Gram-Ve


1 gG,only, crosses placental barrier — others too big. Some

1 gA and I gM in breast milk

b) Reduced antibody response.

5 Intra—ventricular/Peri—ventricular Haemorrhage

a Germinal layer present surrounding Lateral ventricles before about 35 weeks gestation then disappears (Has copious capillary blood supply. Changes in blood flow through capillaries may cause them to rupture - blood into ventricle.

b) Also caused by birth trauma, blood clotting deficiencies.

6 Inability to suck and swallow

Co—ordination of suck and swallow reflexes may not he present before 32 — 35 weeks gestation.

7 Necrotising Enterocolitus

Probable Pathology

Anoxic insult to bowel causes some necrosis to bowel wall — allows bacteria to invade gut, - Peritonitis

Pre—disposing factors:— Birth asphyxia, Umbilical artery catheterization, pre—maturity, Hypertonic feeds (formula feeds). Signs; mucous and blood in stools, abdominal distension and discoloration, bile stained vomiting.

Treatment:- N.B.M. and antibiotics for two weeks.


Those born before 37 weeks of Pregnancy


Skin:- Firm

Thin and friable—opaque

Little sub—cutaneous fat.

Lanugo covering body

Vernix ++

Skull:— Soft

Hair appears on head at 20/40. Very fine, thickens from 37 weeks.

Ears:— (External Ear)

30- 32 weeks - pinna soft, shapeless, stays folded.

33— 37 weeks – Periphery beginning to curl in, returns from folded.

37— 39 weeks - Thin cartilage, Upper border of pinna curved in Springs back.

Term - Firm Cartilage, well formed. Difficult to fold.


30 - 32 weeks - nodule not palpable or visible

32 — 36 weeks — nodule palpable, 2 cms diameter

36 - 38 weeks — palpable 4 cms diameter

39 — 40 weeks — Visible, palpable, 7 cms diameter

Feet:— No sole creases — superficial lines only

Genitalia:— male — Testes not descended before 36 weeks. Scrotum not well developed.

female - Labia minora protrude further than labia majora.

Labia majora small.

Low Birth Weight Infant


Pre—term infant is one born less than 37 weeks gestation.

Low birth weight infants refer to any infant weighing 2.5kg or less at

birth: >>>preterm or SGA.

Very low birth weight Infants are those weighing 1,500kg or less at birth.

Extreme low birth weight Infants are those weighing 1,000kg or less at birth.

Small for Gestational age refers to Infants whose birth weight falls below 10th centile for gestational age.

Characteristics of a L.B.W.I

General Appearance: thin, spindly, maybe very shiny skin, lack of muscle tone.

Position: hypotonic at 28/40 some flexion in lower limbs at 32/40 complete flexion at 36/40.

Head: large in comparison, wide soft fontanels.

Skin: fine, red, shiny, lanugo, blood vessels easily seen, Vernix appears at 28/40.

Breast tissue: not palpable before 34/40.

Cartilage in ears: develops at 35/40, therefore thin pliable.

Chest: small, pliable (recession).

Abdomen: poor muscle tone, therefore appears distended.

Genitalia: Testes undescended, poorly developed scrotum, Labia minora & clitoris exposed due to poor development of labia majora.

Cry: feeble.

Problems of L.B.W.I

1) Birth Asphyxia.

2) Thermal Instability.

3) Lack of primitive survival reflexes — suck, swallow, gag.

4) Jaundice.

5) Pulmonary disease: HMD, BPD, PIE, ITN, Pneumothorax, Pneumonia.

6) Metabolic Disorders: Hypoglycaemia, Hypocalcaemia.

7) Patent Ductus Arteriosus: congestive cardiac failure.

8) I.V.H.

9) Infection.

10) Gastointestinal Intolerance, N.E.C.

11) Opthalmic problems.

12) Surgical lesions, undescended testes.

13) Heamatologiacal problems, D.I.C., Iron deficiency anaemia.

14) Renal Immaturity.

Management of L.B.W.I

1) Resuscitation — Where, by who.

2) Monitor heart rate & respiratory rate.

3) 02 therapy — incubator, head box, ventilation need to measure infant P02 level (arterial 6—lOpa).

4) Monitor blood pressure, mean — 3OmmHg.

5) Thermoregulation.

6) Feeding — E.B.M., Formula Milk — N.G.T., parental feeding — dextrose

7) Jaundice — Prophylactic phototherapy.

8) Vitamins — Konakion at birth


Folic Acid

Vit B


Sytron from 28 days

9) Anaemia, due to frequent sampling at birth (16—20g/dl) slow growth of R.B.C. In bone marrow. shorter life of pre—term R.B.C.

rapid body growth.

10) Handling — remember, rest, stress for infant.

11) Parents — Good liaison parents & nursing/medical staff. parent group BURPS.

Cares & handling


12) Miscellaneous: 3 BM stix

cranial scan

cross infection

hearing tests

baby clinic follow up


S.F.D or I.U.G.R

Follows premature birth as a leading cause of’ peri-natal mortality and increased inter uterine death.

Appearance: Thin - Usually normal length.

Sparse Hair

Dry Skin, Cracked, Inelastic

Muscle Wasting

Little Subcutaneous Fat

Scaphold Abdomen

Thin Umbilical Cord

Wide Eyed and Anxious

Predisposing Factors -



Dysmorphic Features

Twin Pregnancies



Renal Disease

Alcohol Abuse


Low Social Economic Class


Still birth

Fetal Disstress/Asphyxia

Mec Aspiration



Thermal Instability

Skin Infection

Poor Feeding/ Poor Growth

Fetal alcohol Syndrome

Congenital Abnormalities


If premature birth could be stopped there would be a large drop in Mortality Rates.

Definition: baby born before 37 weeks gestation.

Predisposing Factors:

Low Socio Economic Group

Short Stature

No Ante-Natal Care

Previous Terminations


Multiple Pregnancy


Foetal Distress










Neurological Disease

P.D.A. L.B.W. - Light For Dates

Weight at birth below the 10th Centile at that given gestation.

May be: pre-term




Severe growth retardation - slowing of growth as early as the first trimester - is usually due

to: genetic abnormality embryonic injury

viral infection: rubella, CMV, Toxo, etc.


Often die in utero or shortly after birth.

All growth retardation other than above is due to inadequate transfer of nutrition to the infant:

a) Maternal undernutrition or close spacing of infants

b)Maternal or placental disease

- toxaemia

- hypertension

- heart disease

- uterine abn - bicornuate

c) Placental Variations

- multiple pregnancies

- circumvalate placenta

- two vesselled cord.

d) Placental Insufficiency

- ageing of postmature placenta

- placental separation - infarction

e) Placental Infection

- Syphilis

- Toxoplasmosis

- Rubella

- Cytomegalovirus

f Miscellaneous Causes

- Tobacco smoking

- Drug addiction

- Small parents.

g) Genetic Factors

Features of SFD Infants

There are two main groups

1. Long, thin infant - nutritional deprivation in late pregnancy thin and wasted

• LFD infants have a high metabolic rate

• ability to convert amino acids to glucose


Awareness - early Dx

Prevention - early feeding with milk - frequent feeding

Dextrose water - oral or N/G 10-20% Gluc.

IV - 10-15% Gluc. -4 20% - central IV.

Occasionally - very resistant to Rx.

- steroids used.

Congenital Malformations

10-20 times more frequent than AGA infants. No specific form of C.A.’s

- heart

- kidneys


Due to - large surface area and large heat loss

- low substrates i.e. glycogen and fat [ brown fat] for heat production.

Long-Term Prognosis

a) Neurological

Provided free of acute disorders such as:

hypoglycaeinia - especially symptomatic i.e. fits


good prognosis

The infant is able to spare brain damage even in the face of fairly severe nutritional deficiency as evidenced by subcutaneous tissue loss and wasting of musculature. Infants often seem to have enlarged heads on long skinny bodies.

Comparing monozygotic twins - no evidence SFD’s infants perform any worse at school.

b) Very mild forms of growth retardation may catch up especially if COH and length normal.

More severe retardation will show some catch up in first year but then increase parallel to but below the centiles i.e. always short-statured. Head circumference always least affected.

Nursing Care Plan

Small-for-Gestational-Age Newborn


Nursing History

1. Maternal factors:

a. Vascular: pin, chronic hypertension, advanced diabetes.

b. Pre existing diseases: heart disease, alcoholism, narcotic addiction, sickle cell anaemia, PKU.

c. Primiparity, smoking, lack of prenatal care, low socioeconomic level, very young or old.

2. Environmental factors: high altitude, x rays, maternal drug use (antimetabolites, anticonvulsants).

. Placental factors: infarcts, placenta previa.

Foetal factors:

a. Congenital infections.

b. Multiple foetuses.

c. Inborn errors of metabolism.

d. Chromosomal syndrome.

Physical Examination

1. Large-appearing head in proportion to chest and abdomen (asymmetrical SGA).

2. Loose dry skin.

3. Scarcity of subcutaneous fat with emaciated appearance

4. Long, thin appearance.

5. Sunken abdomen.

6. Sparse scalp hair.

7.Anterior fontanelle may be depressed.

8. May have vigorous cry and appear alert.

9. Birth weight below 10th percentile.

Diagnostic Studies

1. Blood glucose and Dextrostix/Chemstrip.


3. Total bilirubin level.

4. Calcium levels.

5. Chest x ray.

Nursing Diagnosis Impaired gas exchange related to aspiration of meconium. EXPECTED OUTCOME: Newborn will show no signs of meconium aspiration.

Observe for worsening signs of respiratory distress such as generalized cyanosis; worsening retractions, grunting, and nasal flaring, evidenced by Silverman-Andersen respiratory index; sustained tachypnea; apnea episodes; inequality of breath sounds; presence of rales and rhonchi.

Administer oxygen per order for relief of respiratory distress signs. Implement treatment plan for respiratory distress.

Monitor blood glucose levels every 8 hr until stable or by Respiratory distress increases consumption of glucose. Dextrostix/Chemstrip within 1—2 hr after birth and frequently for 2—3 days.

OUTCOME MET IF: Newborn’s respiratory rate is 30—60/mm.

• Newborn shows no signs of apnea, intermittent cyanosis, sternal retractions, grunting, nasal flaring, or rales or rhonchi.

• Newborn’s blood glucose levels >40 mg/dL.

Nursing Diagnosis Hyperthermia related to decreased subcutaneous fat. EXPECTED OUTCOME: Newborn will maintain temperature.

Nursing Interventions

Auscultate breath sounds every 4 hr. Suction endotracheal

tube every 3—4 hr. Give oxygen prior to suction as needed.

Ensure chest physiotherapy is done as indicated.


In utero, hypoxia causes relaxation of the anal sphincter with passage of meconium into the amniotic fluid and reflex gasping of meconium. Periodic suctioning maintains airway patency.

Nursing Care Plan

Small-for-Gestational-Age Newborn (continued)

Nursing Interventions

Provide neutral thermal environment range for newborn.

Use skin probe to maintain skin temperature at 36.1 —36.7 C.

Diminished subcutaneous fat and a large body surface com

pared to body weight predispose SGA baby to thermoregulation


Obtain axillary temperatures and compare to registered

skin probe. If discrepancy exists, evaluate potential cause.

Adjust and monitor incubator or radiant warmer to maintain

skin temperature.

Minimize heat losses and prevent cold stress by

1. Warming and humidifying oxygen. Avoid blowing it over the face in order not to increase oxygen consumption.

2. Keeping skin dry.

3. Keeping Isolettes, radiant warmers, and cribs away from windows and cold external walls and out of drafts.

4. Avoiding placing infant on cold surfaces such as metal treatment tables, cold x-ray plates.

5. Padding cold surfaces with diapers and using radiant warmers during procedures.

6. Warming blood for exchange transfusions.

Monitor for signs and symptoms of cold stress:


Newborn’s skin temperature is maintained between 36.1 and 36.7 C.

Newborn shows no signs of lethargy, pallor, or cyanosis.


Newborn will maintain blood glucose levels.

Nursing Interventions

Monitor blood glucose per SGA protocol and report values.

Observe, record, and report signs of hypoglycemia: cyano- Hypoglycemia causes CNS irritability. lethargy, jitteriness, seizure activity, and apnea.

Notify physician if values are low. Monitor vital signs every

2 hr PRN.

Initiate feeding schedule for SGA newborns per agency protocol.

Frequent monitoring of blood glucose assists in identifying decreasing glucose levels.

Provide glucose intake either through early feeding.Provision of glucose through early feedings, or IV.

OUTCOME MET IF: • Newborn’s blood glucose is greater than 40 mg/dL

Newborn shows no signs of cyanosis, lethargy, jitteriness, seizure activity, or apnea.

Nursing Care Plan.

Small-for-Gestational-Age Newborn (continued)

Nursing Diagnosis Altered nutrition: less than body requirements related to SGA’s increased metabolic rate.

EXPECTED OUTCOME: Newborn maintains or gains weight.

Nursing Interventions

Initiate test water feeding at 1 hr of age, then proceed to 5% glucose/water. Move early to formula feeding every 2—3 hr.

Supplement oral feedings with intravenous intake per physician order.

monitor I/O every 4 hr or more frequently.

Use concentrated formulas that supply more calories in less

volume, such as Similac 24.

Promote growth by providing caloric intake of 120—150

kcal/kg/day in small amounts. Monitor and record signs of

respiratory distress or fatigue occurring during feedings.

Supplement gavity, bottle-, or breast-feedings with intravenous therapy per physician order until oral intake is sufficient to support growth.

Begin bottle- or breast-feeding slowly, such as once per day,

then once per shift, then every other feeding.

Monitor daily weight with anticipation of small amount of

weight loss when bottle- or breast-feedings start.

OUTCOME MET IF: • Newborn does not lose more than 2% per day of body weight.

• Newborn receives and tolerates 120— 150 kcal/kg/day.

• Newborn takes formula without tiring.

Nursing Diagnosis Altered tissue perfusion related to increased blood viscosity.

EXPECTED OUTCOME: Newborn will show no signs of complications from increased blood viscosity.

Nursing Interventions

Obtain central hematocrit on admission.

Monitor, record, and report symptoms, including:

1. Decrease in peripheral pulses, discoloration of extremity, alteration in activity or neurological depression, renal vein thrombosis with decreased urine output, hematuria, or proteinuria in thromboembolic conditions.

2. Tachycardia or congestive heart failure.


Sterile water is desirable for first feedings because it causes fewer pulmonary complications it aspirated into the lungs.

SGA newborns require more calories/kg for growth because of increased metabolic activity and oxygen consumption secondary to increased percentage of body weight made up by visceral organs.

Small, frequent feedings of high caloric formula are used because of limited gastric capacity and decreased gastric emptying.

Adequate nutritional intake promotes growth and prevents such complications as metabolic catabolism and hypoglycemia.

Gravity feedings require less energy expenditure on the part of the newborn.

Bottle- or breast-feeding and active rather than passive intake of nutrition require energy expenditure, burning of calories, and potential weight loss.


Polycythemia is defined as a central venous hematocrit above 65—70% in the first week of life. Hyperviscosity is resultant thickness and decreased deformability of red-cell rich blood so that its ability to perfuse the tissues is disturbed. Exact etiology of polycythemia in SGA is not known but is thought to be a physiologic response to chronic hypoxia with increased erythropoietin production.

Small-for-Gestational-Age Newborn (continued)

Nursing Interventions

3. Respiratory distress syndrome, cyanosis, tachypnea, in creased oxygen need, labored respirations, or hemorrhage in respiratory system.

Watch for other signs of increased hematocrit, such as hyperbilirubinemia. Monitor bilirubin levels every 8 hr.

Assist with partial plasma exchange.

OUTCOME MET IF: . Newborn’s hemoglobin is less than 22 g/dL.

Newborn’s hematocrit is less than 65%.

Newborn shows no sign of cyanosis, tachypnea, labored respirations, or hyperbilirubinemia.

Nursing Diagnosis Altered parenting: high risk related to prolonged separation of newborn from parents secondary to illness.

EXPECTED OUTCOME: Parents will demonstrate evidence of positive physical and social interaction with newborn.

Nursing Interventions

Include parents in determining infant’s plan of care and en courage their participation. Encourage parents to visit frequently. Provide opportunities for parents to touch, hold, talk to, and care for their infant. Determine the type and amount of appropriate sensory stimulation and implement sensory stimulation program.

OUTCOME MET IF: . Parents demonstrate two or more of the following physical interactions: good eye contact, touching baby, holding baby close, attempting to comfort baby, kissing baby.

Parents demonstrate two or more of the following social interactions: calling baby by name, making positive comments about baby, asking questions about baby, asking questions about newborn care, talking to baby.

Knowledge deficit related to lack of information about care of newborn at home. EXPECTED OUTCOME: Parents will be able to manage newborn care at home.

Nursing Interventions

Prepare for discharge by instructing parents in such areas as feeding techniques, formula preparation (including bottle sterilization), and breast-feeding; bathing, diapering. hygiene; temperature monitoring; administration of vitamins; sibling rivalry; care of complications and preventing exposure to infections; normal elimination patterns, expected weight gain patterns, normal reflexes and activity, and how to promote normal growth and development with out being overprotective; returning for continued medical care; and availability of community resources if indicated.

OUTCOME MET IF: Parents verbalize/demonstrate ability to care for newborn at home, when to return for fol. low-up visits; what signs and symptoms to report to health care provider; and available community resources.


As the increased red blood cells begin to break down, hyper bilirubinemia may present.

Partial plasma exchange decreases blood volume and blood viscosity to less than 60%.

Parent-infant bonding begins in the first few hours or days following the birth of an infant. SGA infants experience prolonged periods of separation from their parents. Which necessitates intervention to ensure parent-infant bonding.

Emotional support of the psychological well-being of the family, including positive parent-infant bonding and sensory stimulation of the infant, is important.

Parents should receive the same postpartum teaching as any parent taking a new infant home. Parents need to understand the changes to expect in colour of the infant’s stool and number of bowel movements, plus odour from bottle- or breastfeeding, to avoid unnecessary concern. Preterm infants usually do not require referral to community agencies unless there is a specific problem requiring assistance. Infants with Congenital abnormalities, feeding problems, or resolving complications with infections, or mothers unable to cope with defective infants, may require referral to community resources.


Visible discolouration of skin and conjunctiva as a result of excess bilirubin in plasma and tissue fluids.

Normal values:

Adult 17 - 35 mmol/lt

Average 23 mmols

Newborn35 mmols

Visible at 120 mmols

Bilirubin Metabolism

RBC broken down — Haemoglobin(globin + iron stored) = Bilirubin - transported in blood attached to albumin as unconjugated bilirubin (fat soluble) blood brain barrier is penetrated.

Arrives in liver where in presence of enzyme gluconyl transferase is

conjugated (water soluble)

Excreted in bile


Albumin Binding Problems

a) Low albumin level in preterm

b) Drugs, eg. indomethacin, frusemide, steroids

C) Intralipid

d) Acidotic


Presence of unconjugated SBR inhibits enzymes within brain tissue.

Causes: Poor feeding, lethargy, vomiting

— Febrile, restless, head retraction

— Fits, death

- Cerebral palsy


Physiological Jaundice

1.Increased RBC mass

Delay cord clamping

Twin to twin transfusion

Polycythemia (1DM)

Maternal/fetal transfusion

2.Decreased RBC survival

Full term90 days

Pre term40 days

Adult 120 days



4.Immature Liver

High Hb

Conjugation inadequacies


5.Breast Feeding

Inhibition of GT by a steroid

Pregnane found in breast milk

Pathological Causes


Rhesus incompatibility

ABO incompatibility

Other red cell anomalies


Enzyme disorders, glucose & phosphate


Thalassaemia/sickle cell


2.Gluconyl Transferase del

Cragler Najar Syndrome

3.Impaired Excretion

4.Mixed conjugated unconjugated

a) Metabolic - Cystic fibrosis


b) Infective - Hepatitis


6.Enterohepatic circulation

Paralytic ileus

Bowel obstruction


1. Ante-natal detection Rh neg women screened

2. Amniocentesis if 1’ levels of Anti 0 antibody present.

3. Plan delivery with Paediatrician and Obstetrician

4. Cord blood - Group OCT SBR Hb

5. Regular SBR and phototherapy

6. Exchange transfusion

7. Intra-uterine transfusion

Prevention of HDN

Giving Anti D following delivery 72 hours.

Kleihauer test

Spontaneous abortion




External cephalic version

Thermo regulation in the newborn

Humans are homeothermal, and maintain a constant core temperature of 37C independent of the environment.

Heat gain in adults

Metabolism is a major source of heat gain.

The liver produces a constant amount of heat, the skeletal and cardiac muscles produce heat, this varies according to the amount of exercise being undertaken.

In total the body can generate around 1’C per hour at rest.

Heat can also be gained from the external environment, such as from hot food and drink, but this is minimal.

The ingestion and digestion of food however, particularly fats and proteins increase metabolic rate, and therefore temperature.

Heat loss

Heat is lost in four ways, conduction, evaporation convection and radiation. 15% of heat loss is through urine, faeces and the respiratory tract.

Temperature control

Temperature is controlled by the hypothalamic heat regulating centre in

the brain.

In heat

The adult has several behavioural responses. Maximum body surface is exposed, an open body posture being taken.

Less exercise is taken, apparent lethargy.

In cold

Behavioural responses are to increase activity, and reduce exposure of body surfaces.

Shivering, is unco-ordinated muscle activity, which is triggered by cooling the body surface below 28°C. It is not a sustained activity, but can increase the basal metabolic rate by three times. It is controlled by the shivering centre in the hypothalamus, influenced by the anterior heat regulating centre.

The hormones thyroxine, Adrenaline and noradrenaline are released, to increase the metabolic rate. The peripheral circulation is reduced, by, vaso-constriction.

The normal newborn

The normal newborn infant has a large surface area for a small body mass, and looses heat rapidly. The smaller the infant, the greater this loss, particularly if he is naked. The baby has limited subcutaneous fat deposits to provide insulation, he has a limited metabolic capacity, and vasomotor instability.

Defences against hypothermia.

Vasomotor control

The neonate conserves heat through vasoconstriction, and dissipates heat through peripheral vasodilation.

Thermal insulation

Provided by subcutaneous white fat. Commonly accounts for 11 - 17 % of full term neonates weight.

Muscle activity.

Initially the neonate will react to cold with increased movement, this can be perceived as irritability. The infant may adopt a tightly flexed posture in order to conserve heat. Whether the newborn can shiver or not is open to debate, even if shivering does occur in response to severe cold stress, it does not serve as a major heat source.

Nonshivering thermogenesis

The production of heat by the lipolysis of brown fat.

Brown fat is a type of adipose tissue which accounts for 1.5% of a full term neonates body weight. Brown fat is found around the neck, head, heart, great vessels, kidneys, and adrenal glands; behind the sternum; and in the axillae. In response to heat loss noradrenaline is produced, this hormone stimulates the oxidisation of brown fat. Heat produced by brown fat oxidation is distributed throughout the body by the blood, which absorbs heat as it flows through fatty tissue.

Thermo-neutral environment

As oxygen is used in an infants efforts remain warm, or when he is hot and restless, the ideal thermal environment will be one where the infant’s oxygen consumption is minimal. Several charts are available which indicate the correct environmental temperature in which to nurse a neonate.

Small and sick neonates

If problems of heat regulation are encountered by normal newborns, so much are the problems compounded for sick and small babies. Some of the problems associated with unstable temperatures arc listed by Roberton (1993)

Effects of cold

Decreased surfactant synthesis, and efficiency


Increased oxygen consumption

Diversion of cardiac output to brown fat

Increased use of calorie reserves

Neonatal cold injury

Increased postnatal weight loss and slower weight gain

Disseminated intravascular coagulopathy

Increased neonatal mortality and morbidity

Effects of heat

increased fluid loss

Hypernatraemia (sodium pump)

Postnatal weight loss


Recurrent apnoea

Neonatal mortality and morbidity.

Care of a baby to prevent temperature instability

1. Initial care

Keep baby warm at delivery.

Transfer baby in transport incubator.

Ensure platform or incubator preheated.

Use servo-control.

Ensure early feed, or I.V. fluids.

Prevent hypoglycaemia.

Be aware of thermo-neutral environment.

Humidify all gases.

2. Follow on care

Regular checking of axilla temperature. Including on


Use air temperature as soon as possible.

Use of humidity if baby nursed naked.

Use of plastic sheeting humidity in very small babies.

Reduce number of interventions.

Dress babies as soon as possible.

Encourage Kangaroo care/skin to skin contact.

Positioning to prevent heat loss.

If baby is cold

Is incubator temperature high enough-check chart?

Is servo probe attached firmly?

Is humidity working/water tank empty?

Is he wet, Nappy/sheets/blankets?

Has he been out of incubator/platform or bathed?

If baby is hot

Is incubator temperature set too high - check chart?

Is servo probe attached firmly?

Is humidity set too high?

Is baby wearing too many clothes?

Is baby under phototherapy?

Is baby lying in direct sunlight?

What to do

If temperature is below 36.7C or above 37AC look at check list

remedy any obvious problem.

Recheck temperature in 1 hour.

If still out of normal range ask for help.

What might be wrong

The baby may have an infection, this is often indicated by an unstable temperature rather than a pyrexia, especially if associated with general lethargy.

The baby may be dehydrated. This often occurs in term babies who have fed poorly. Rehydration is often the cure.

Brain damage, with injury to the hypothalamus.


Cleft Lip and Palate

Remember to check carefully for evidence of other abnormalities - 7% have heart problems, though only about 1% are part of multiple malformation syndrome. If in doubt - get advice!


Ensure that parents understand that circumcision must NOT be carried out as foreskin needed for subsequent repair.

Undescended Testes

If bilateral consider checking chromosomes as may be verilised female.

Unilateral - likely to descend in first year. Ask parents to ensure checked by GP at that time so surgical referral can be arranged if required.


Very common. Reassure parents of spontaneous resolution. If persist, GP can arrange referral.

Accessory Digits/Skin Tags

Do NOT tie off yourself.

Heart Murmurs

If seem significant, discuss with Registrar. Chest x-ray, ECG or clinic follow-up may be required.

Congenital Talipes Eguinovarus

If mild and positional, ward staff will refer directly to Physiotherapists.

If not positional, requires orthopaedic review and referral directly to Physiotherapy.

Discuss with Registrar.

Check carefully for associated anomalies, eg. dislocated hips, dysmorphic features suggestive of a syndrome.

NB - If unsure of correct producure, always ASK!

Screening for Developmental Dysplasia of Hips

Family history

Breech presentation

Clicky (not unstable) hips

"Clicky Hips" - If merely clickly - Hip Ultrasound Scan at six weeks of age.

If unstable or dislocated, needs orthopaedic review - discuss with Registrar


Family history of early onset deafness

Cleft lip/palate

Abnormalities of external ear including pre-auricular skin tags

Syndromes, eg. Downs Syndrome

Antenatal Renal Tract Abnormalities

Ensure that baby has no other associated abnormalities and is passing urine.

Request repeat renal ultrasound, usually after first five days of life, to ensure adequate urine production to show reflux, etc.

UNLESS potentially serious malformation, eg. polycystic kidneys, gross hydronephrosis on antenatal scan, possible posterior urethral valves

OR poor urine output, vomiting, etc.

THEN request early scan, check U & Es and creatinine, BP, urine culture and starting Trimethoprim may be appropriate

DISCUSS with a senior colleague

NB: Ensure that the baby’s GP is informed of all significant abnormalities or postnatal problems

Erbs Palsy

Refer to (Orthopaedic Surgeon). He may be able to see them on postnatal ward or early clinic after discharge. He will also see other upper limb abnormalities but ask for senior review prior to referral.


No need for Baby Clinic follow-up.

If high risk (eg. both parents heterozygotes - or mum heterozygote and father’s status unknown) they will have requested cord blood testing and will arrange appropriate care.

If low risk, ie. baby either heterozygote or normal, family can be offered blood test for baby at four months.


A screening procedure, should fulfil the following criteria (WHO):

- The condition is such that it should be an important problem.

- There should be an accepted treatment for recognised disease.

- Facilities for diagnosis and treatment should be available.

- There should be a recognised latent or early symptomatic stage.

- There should be a suitable test or examination.

- The test or examination should be acceptable to the population.

- The natural history of the condition, including its development from latent to declared disease should be understood.

- There should be an agreed policy on whom to treat as patients.

- The cost of case finding (including diagnosis and subsequent treatment of patients) should be economically balanced in

relation to the possible expenditure on medical care as a whole

- Case findings should be a continuing process and not a once for all project.

Early asymptomatic diagnosis, such as phenylketonuria by way of Guthrie Test, enables treatment to be carried out before irreversible damage has occurred. There are very strong economic arguments also in favour of the strategy of this type of screening phenylketonuria and hypothyroidism. The complete epidemiological data is not available for the population of premature infants most at risk for Retinopathy of Prematurity but it see likely that most of the above criteria would be fulfilled from information that is available at present.

An ideal screen test should be rapid and simple to apply and a reliably distinguish between those who have the condition and those who do not.

Sensitivity and Specificity

Sensitivity is the ability of a test to identify correctly those who have the disease.

Specificity is the ability of a test to identify correctly those who DO NOT have the disease

Retinopathy of Prematurity

The retina is the innermost layer, and part of the central nervous system. It is an offshoot of the brain.

It contains the visual cells which respond to light. (Rods and cones,)

The blood supply to the retina is from both surfaces, the retina being sandwiched between the choroid outside, and the retinal circulation inside. As with the cells of the brain ‘grey matter’, the retina has a very high and constant demand for oxygen.

The retina has two specialised areas.

1. The optic disc.

Is where the ganglion nerve fibres of the retina converge (blind spot)

and leave the eye as the optic nerve. Here the retinal blood vessels enter the eye.

2. The macula lutea. (Yellow spot)

Is that part of the retina directed at the object of visual attention, has the

highest acuity, and lies on the visual axis which is the line of directed

vision passing through the object of visual attention. It contains cones,

but no rods. Its function is assisted by:

a) Absence of blood vessels anterior to the macula.

b)Macular retina is thinned into a depression (the fovea centralis)

c) Each cone has a separate ganglion cell; elsewhere as many as 200

visual cells connect through to each ganglion cell.

The physiology of retinopathy of prematurity

The pathophysiologic process is not fully understood. Many factors play a role in the pathogenesis. It has been known since the 1950s that oxygen therapy and blindness in premature babies was linked. It seems that when hyperoxia is involved, that it is the pressure in arterial blood Pao2 than the concentration of administered oxygen (F102) that is important.

In response to hyperoxia the retinal vessels constrict. They may permanently constrict and become necrotic (vaso-obliteration). The vessels that have not been obliterated may proliferate in an attempt to re establish retinal circulation. Proliferating vessels may extend into the vitreous, causing fluid leakage and/or haemorrhage, with retinal scar formation, traction on the retina, detachment and blindness.

The degree of retinal vascularisation at birth determines the suceptiblity to the insult of hyperoxia.

This is mostly achieved by 32 weeks of gestation.

Nursing care

Prevention is better than cure! A careful monitoring of Pa02, which should be kept below 12 KPa which is thought to be the danger level.

An awareness of the screening programme.

As a named nurse ensuring your baby is screened and followed up as necessary.


Retinopathy of prematurity, (ROP) formerly known as retrolental fibroplasia, is a disorder occurring in the developing retina of newborn babies, usually in premature - infants. It is a disorder of vasoproliferation and the incidence increases significantly with immaturity and low birth weight.

It can regress spontaneously, but can progress to significant vasculogenesis with the newly proliferated blood vessels branching into the vitreous gel. This may lead to retinal dragging and detachment.

It is a complex multifactorial disorder.

A direct association between 02 dosage and the development of retinal abnormalities has been identified, but the relationship between Oxygen and retinopathy is more complex than was originally thought. Some infants will develop ROP despite never having received supplemental oxygen whilst others can sustain high levels of the gas without developing retinal changes.


Immaturity - the most consistently recognised risk factor

Oxygen - The risk of development of ROP is generally related to both the 02 concentration and the duration of oxygen therapy.

Blood Transfusions - Top up transfusions with adult blood cause a shift in the oxygen dissociation curve so that more oxygen is given up for a particular PO2, thereby exposing the retina to higher oxygen levels.


Clinically, by indirect opthalmoscopy after insertion of eye drops e.g. 0.5% cyclopentolate to dilate the pupils. Examination is performed by a paediatric ophthalmologist.


* Stage 1 - thin line of demarcation in the periphery of the retina separating the avascular retina from the vascular retina posteriorly.

* Stage 2 - the line is more extensive and forms a ridge

* Stage 3 - vascular proliferation immediately posterior to the ridge

* Stage 4 - complete detachment of the retina.

Stages 1 & 2 normally regress completely to normal

Stage 3 may require treatment.


Screening at 32 weeks

* Monitoring of oxygen in sick newborn infants. Maintain P02 at 6-8kPa

* Supplementation with vitamin E possible preventative measure - not used in UK

* Treatment is controversial - Cryotherapy (invasive treatment)

Laser therapy more commonly used.


All babies born in the UK should be screened for PKU (phenylketonuria) and congenital hypothyroidism (cretinism). Parents can refuse this test but this must be recorded and the General Practitioner notified. It is possible that in the near future the screening program will be extended to include testing for CF (cystic fibrosis).

The timing of the blood collection is not critical but two points must be considered:

1) If screening is done too early the TSH surge which occurs at birth and is not normalised until the first 3 to 4 days of life may give a falsely elevated level on screening. Similarly if the child has not had milk feeds any inability to handle protein may be missed since the child is not effectively using normal metabolic pathways.

2) If screening is left too late some mental damage may already have occurred before the result of screening and confirmation tests are available and therapy instituted.

In general a window of 6 to 14 days after birth is available in which to collect the specimen. This allows time for delivery to the laboratory, analyses to be performed and any abnormality be detected sufficiently early, (before 21 days), to allow effective therapy to be instituted.

When the screen was introduced blood collection was done by the Health Visitors and consequently could not be done before 10 days. Now the system has changed and Midwives collect the blood earlier collections are possible. Going too soon however means the baby will be less easy to bleed and the parents less amenable to any distress which the blood collection may cause.

In this country blood collection takes one of two forms. Either blood is absorbed onto special filter papers (Guthrie cards) as dry blood spots or collected anti coagulated and sent to the laboratory in liquid form in a suitable container. The initial reason for using dry blood spots was simply for stability since the specimen often had to be transported over long distances from remote collection points to large central screening laboratories. This of course could take several days in the post. In England, where distances are often small, the use of liquid blood is much more generally viable although clearly delays longer than several hours can invalidate results. In both situations cool storage of a specimen is important and in particular leaving specimens in hot cars can be a problem.

Analysis of the specimen to detect hypothyroidism consists of measuring TSH (Thyroid Stimulating Hormone). TSH is a Hormone produced by the pituitary gland which stimulates the Thyroid to produce thyroxine (T4) and tri-iodothyronine (T3). These two hormones are then responsible for controlling metabolic activity at cellular level. Under normal conditions as T4 and T3 are produced they have an effect on the pituitary which lowers production of TSH. This consequently lowers production if T4 and T3 which then causes the Pituitary to again increase TSH production. This results in a finely balanced and steady state production of all three hormones.

In cases of partial or complete hypothyroidism the thyroid gland cannot produce T4 and T3 so the TSH production from the Pituitary is never suppressed. Consequently levels of TSH in the patient’s blood remain high and levels of T4 and T3 remain low. Detection of high levels of TSH in neo-nates therefore are indicative, but not diagnostic, of hypothyroidism. Like all screening programmes the screening test must be confirmed by back-up diagnostic tests. The methods used for measuring thyroid hormones are all based in immunoassay techniques using isotopic or fluorescent labels as reaction monitors.

PKU occurs in babies who are born with a defective enzyme called phenylalanine. Hydroxyls. This enzyme is responsible for converting phenylalanine to tyrosine. If the enzyme does not fulfil its role the phenylalanine concentration builds up in the baby’s blood and can then be detected as an abnormally high level. As the level increases it is converted to phenypyruvic and phenyllactic acids which are keto-acids excreted in the urine and hence the name phenylketonuria. It was the detection of these compounds in urine which formed the basis of the early screening programes (ketostix). However high levels of these acids in the blood before excretion can cause irreversible brain damage and consequently the sooner the problem is detected the sooner treatment can be implemented and risk of damage minimised.

Detection of PKU can be done in one of several ways

using either blood spots or liquid plasma:

1. Microbiologically (Guthrie test).

2. By chemically measuring phenylalanine specifically either directly on plasma or after

extraction of plasma from blood spots.

3. By chromatographic examination of all amino acids in the specimen.

1. The Guthrie test has been the principal test for PKU. The blood spot is placed on a culture plate in which the growth of specific bacteria is influenced by the amount of phenylalanine present. This approach can be used for several other blood constituents but each one requires bacteria of specific characteristics the growth of which will be modified by atypical concentrations of amino acids present in the patients blood. Each different amino acid to be checked will therefore require a separate blood spot and several different bacteria will be required to cover the range of amino-acids to be checked.

2. The chemical method is probably the simplest and is usually based, on the the measurement of fluorescence when phenylalanine undergoes chemical reaction. This procedure has only been applied to phenylalanine but has the advantage of being readily automatable and therefore very applicable to large numbers. If the specimen is presented to the laboratory as a blood spot an extraction stage has to be undertaken before the analysis can be performed. This approach however will only detect PKU and none of the other aminoacidopathies.

3. The Scriver test, which is based on a TLC (thin layer chromatography) procedure and can be done on either liquid plasma, or on plasma extracted from blood spots. A small volume of specimen is applied to the bottom of a thin layer of cellulose coated on an aluminium support. The plate is then placed in a small volume of solvent and as the solvent moves up the plate by capillary action each amino acid eventually lies as a discrete band because of the selective solvency of different amino acids, . After drying the plate the amino acids can be visualised by staining with Ninhydrin. This technique has the great advantage of allowing examination of the specimen for a whole range of amino acid abnormalities at one time. Thus abnormalities such as Maple syrup urine disease, Tyrosinaemia, Histidinaemia, and others can all be tested for at one time.

Whichever test is used co-operation and understanding between laboratory and collectors is essential. It is important that the Laboratory appreciate the difficulties involved in collecting blood from tiny babies under what may be less than ideal circumstances and similarly it is important to appreciate that analysing small volumes of blood presents difficulties. The very nature of screening programmes means that equivocal results and requests for repeats is inevitable. Success is down to the fact that there has been a good, close working relationship between all people involved in the screening programme.

Summary of recommended screening procedures and assessments.

Neonatal examination

• Review of family: history, pregnancy and birth.

• Discuss any concerns expressed by the parents.

• Full physical examination, including weight and head circumference.

• Check for congenital dislocation of the hips.

• Check for testitcular descent.

• inspect eyes.

• Examine eyes for red reflex.

• If high risk of hearing defect—refer for further testing. blood tests for penylketonuria and hypothyroidism.

The examination is normally carried out within forty- eight hours of birth and again before discharge. It usually includes:

• Weight

• Head circumference

• Skin—for colour. birthmarks, etc.

• Head shape

• Fontanelles

These. with the majority of children, will be carried out in hospital by a paediatrician or obstetrician before the child is discharged. However, the neonatal examination is an extremely important part of overall child health surveillance as the majority of severe abnormalities are picked up at this time.

Child health: the screening tests

• Ears

• Eye appearance, including red reflex

• Palate—hard and soft

• Heart—auscultation

• Pulses

• Respiratory system

• Abdomen

• Umbilicus

• Genitalia— descent of testes in boys

• Limbs—for normal formation, tone, and movement

• Anus—normal appearance

• Hips—for congenital dislocation.

Phenylketonuria — (approximate incidence 1:10 000 live births)—blood normally taken by heel prick 6-10 days after birth.

• For congenital hypothyroidism (incidence 1:3500)—blood

normally taken at same time as blood for phenylketonuria.

6-10 days after birth.

Screening for congenital dislocation of the hip

1. Introduction

Congenital dislocation of the hip (CDH) is a potentially crippling disorder associated with a high degree of handicap and orthopaedic problems in childhood and adulthood if not recognized early.

2. Incidence of CDH

The incidence of CDH in Caucasians is about two in every thousand live births. The incidence of hip instability is how ever, ten times as high as this: and although the majority spontaneously become normal, screening techniques cannot distinguish between those cases which will and those which will not resolve, Waiting for the natural evolution and postponing treatment is wasting time. and the outcome deteriorates. The earlier the diagnosis and treatment the better the outlook.

3. Aetiology and risk factors

Aetiology of CDH s still unclear.

Risk factors associated with an increase of incidence:

• genetic —familial history of CDH


• gestational—oligohydramnios

—uterine malformations

—first baby

—foetal growth retardation

— breech presentation

— Caesarean section

• Other congenital malformation (especially of the foot)

4.Screening tests

Modified Ortolani – Barlow manoeuvre The following conditions must be followed;

1. The infant must be undressed from the waist downwards.

2. The examiner: hands should be warm. The examination gentle and the baby relaxed.

3. The infant lies on his/her back with legs towards the examiner, and the hips abducted and fully flexed.

4. For examination of the left hip the examiner steadies the infant’s pelvis between the thumb of his left hand, on the symphysis pubis, and the fingers. under the sacrum.

5. The upper thigh of the left leg is grasped by the examiners right hand, with the middle digit over the greater trochanter, with the flexed leg held n the palm, and with the thumb on the inner side of the thigh opposite the lesser trochanter.

6. An attempt is now made to move the femoral head in turn gently forwards into and backwards out of the acetabulum.

7. In the first part of the manoeuvre the middle digit is pressed upon the greater trochanter in an attempt to relocate the posteriorly displaced head of the femur forwards into the acetabulum. If the head is felt to move usually not more than 0.5 cm with or without a palpable and or audible clunk then dislocation s present.

3. The second part of the manoeuvre tests for instability. With the thumb on the inner side of the thigh, backward pressure is applied to the head of the femur. If the latter is felt to move backwards over the labrum (the fibrocartilagineous rim of the acetabulum) on to the posterior aspect of the joint capsule (again a movement of not more than 0.5 cm, and often accompanied by a ‘clunk) then the hip is said to be subluxatable or unstable.

9. To examine the right hip the role of the examiners hand is reversed.

‘b) Abduction test

This test should be carried out at all ages, as limitation of abduction is the most important sign of dislocation.

With the infant lying on his her back and hips flexed to 90 degrees:

1. either both hips can be abducted at the same time—with limitation noted in one hip or the other, or both in bilateral dislocation (thighs normally abduct to 75o) or

2. One hip at a time can be abducted; but the pelvis must be stabilized with the other hand to prevent ‘tipping’.

5. Classical signs

1. Imitation of hip abduction (persistent and less than 75°),

2. Shortening of the leg on the affected side and asymmetry between the two sides. (With hips flexed, compare knee levels. it is an above-knee shortening.)

3. Asymmetrical skin creases; check in supine and prone positions (not very reliable, but it can help the diagnosis).

4. Flattening of the buttock on the affected side in the prone position.

5. Leg posture: the affected side tends to be held in partial lateral rotation, flexion, and abduction.

Screening for visual problems

1. Introduction

Although the most serous visual defects are usually apparent at the neonatal examination or subsequently become evident to the parents. screening for visual impairment is essential for the identification of the less serious but more common problems.

2. Prevalence of some visual defects in childhood (per 1000 live births)

• squint—30-40 1000

• hypermetropia—30. 1000

• astigmatism—30 1000

• myopia— 10 (6 years) to 200 (16 years)/ 1000

• cataract—O.2 (bilateral)+ 0.2 (unilateral)/ 1000

• optic atrophy—0.2/ 1000

• retinoblastoma—O.l/ 1000

• colour vision defects—80/ 1000 boys

— 4/ 1000 girls

• amblyopia—20 (in general population)/ 1000

• (disabling visual impairment is present in 2-4/ 10 0003.Aetiologies and risk factors

Causes of severe visual handicap in children

• congenital conditions (inherited ,disorders of the eye or multiple malformative syndromes, prenatal infections rubella, etc.)—70 per cent

• optic atrophy— 10 per cent

• retrolental fibroplasia—6 per cent

• retinoblastoma—4 per cent

• Other (postnatal eye or brain infection or trauma, prenatal insults)—10 per cent

Risk factors associated with an increase of visual problems

• Familial history of—squints

—ocular disorders before six years

—wearing glasses before ten years

—retinoblastoma, glaucoma, etc.

• Prenatal infection—rubella

•prenatal insults

• Recognisable genetic syndromes and other malformations

• Postnatal infections (eye or brain)

• Trauma (head or eye)

• Oxygen therapy in the neonatal period

• Child abuse (head-shaking)

4. The tests

(a) History

• Check risk factors (see above)

• does the mother think the child sees normally?

• Is the mother worried about the child’s eyes?

(b) Ocular appearance

• Do the child’s eyes look normal? 15 the gaze steady?

(C Ask about any parental concern

(D,) Active questioning of parents:

Does the baby:

• look at the parents?

• follow moving objects with the eyes?

• fixate small objects?

6. Action


• If there is any concern about the child’s vision

• If risk factors are present

1. Introduction

All long-standing bilateral hearing impairments in children are significant because they may adversely affect the child’s linguistic, educational, social, and emotional well-being by preventing the acquisition of normal language, and thus also obstructing normal social interaction.

Early diagnosis is therefore essential.

2. Prevalence of bilateral sensor neural hearing impairment in children:

• mild (35-50 dB)—l3/ 1000 children;

• moderate (50-70 dB)—2/ 1000 children;

• severe (>70 dB)—1/ 1500 children.

(Twenty five per cent of children under five years, and five to ten per cent of those over five years experience some transient conductive hearing-loss at some time.)

3. Aetiological factors

Children at increased risk of deafness

(These factors appear in 8 per cent of all children. and include 70-80 per cent of those with early deafness.)

• Family history of hereditary childhood deafness;

• rubella, flu, or other prenatal non-bacterial infections the first trimester of pregnancy;

• physical malformations. especially around the ear;

• prematurity;

• severe neonatal jaundice;

• drugs (aminoglycosides);

• meningitis, encephalitis, mumps, or measles;

• cerebral palsy;

• recurrent otitis media;

• head injury;

• birth asphyxia; and

• facial malformations. or Down s or Turners syndrome.

4. Main causes of hearing-loss

(a) Conductive hearing-loss

Conductive hearing-loss is caused by mucous secretions (glue’) accumulating in the middle ear. This occurs as a result of blockage of the Eustachian tubes. These secretions interfere with the normal movements of the ossicles and ear drum; the condition is called secretory otitis media (SCM).

Children with Downs syndrome. Turners syndrome. facial malformations, or cleft palate. are at particular risk of developing a conductive hearing-loss.

• Note—wax does not normally cause hearing-loss in children.

Sensor neural hearing-loss

This can be congenital or acquired. The inner ear (cochlea) or the nerve pathways are damaged. The hearing-loss is profound and permanent.

(C) Mixed conductive and sensor neural hearing-loss

(a) Utilization of parental suspicion

Parents’ observations of their babies’ reactions to sounds are very reliable indicators for the diagnosis of hearing problems—this can be aided by the parents having a check-list to complete about their observations of their child’s response to sounds (McCormick 1988).

Ask parents if hey have any concern about their childs hearing.

• Check for risk factors.

• Note if parents mention that the child:

—makes a limited number of sounds:

—screams in a high-pitched voice:

—has a funny voice;

—doesnt turn towards sounds:

—has an absence of the startle reflex between birth and four months: or

—shows the presence of the startle reflex between four months and one year.

Children should have a hearing test any time that the parents or anyone else is concerned as to whether the child can hear or not.

Refer to GP. for ear examination and further management

Fig. 8.2. The action sequence screening for hearing problems.

When to refer.

1, Refer mmediately to ENT via the GP if the baby; child appears to be profoundly bilaterally deaf.

2. Do not omit standard referral procedure if the baby child has a cold during the two tests.

3. If a baby child fails the hearing test on the re-test the ear drums should be examined and appropriately treated. If the baby child has bilateral serous otitis a referral to ENT or to Audiology may be indicated.

4. Direct referrals from health visitors can be made to hearing therapists in ENT with GP consent.

Screening for heart disease_

1. Introduction

It is important that doctors involved in surveillance can distinguish between innocent and pathological murmurs, and are able to identify the other signs and symptoms of congenital heart disease (CHD).

2. Incidence

Six to eight children in a thousand are born with congenital heart disease. However, an innocent or physiological mur mur is present in more than 50 per cent of all children and adolescents.

3. Aetiology and risk factors

The aetiologies of congenital heart diseases are numerous and usually unknown; but some risk factors that are associated with a higher incidence of CHD are:

(a) family history of CHD or other malformations (ie. renal);

(b) pregnancy problems (infections, X-ray, alcohol, tobacco, drugs, drug abuse, systemic diseases, etc.);

(c) birth problems (low or high birth weight, anoxia, resuscitation);

(d) neonatal problems (infection, respiratory); and

e) recognizable genetic syndromes or other malformations.

4. Age at examination

At birth, at from six to eight weeks, and opportunistically up to four and a half to five and a half years, at which age examination should be carried out on school entry.

5. Symptoms which should alert the examiner

1. Shortness of breath on exertion.

2. Chest pains.

3. Excessive tiredness.

4. Palpitations or syncope.

5. Feeding problems and or failure to thrive.

6. Late walking.

7. Excessive sweating.

8. Squatting.

9. Recurrent low-respiratory-tract infections.

6. Examination

(a) The murmur

A murmur should be listened to:

1. Standing or sitting and supine.

2. In inspiration and expiration.

3. Over the left and right of the front chest, the back, and the neck.

4. If a murmur is continuous and is transmitted to the neck, listen with the child supine with his her legs higher than his/her head. If the murmur is a venous hum the diastolic component will disappear.

Innocent murmurs are commonly:

1. Systolic with no diastolic component (except venous hum).

2. Soft, graded

3. Short ejection murmurs.

4. Well localized without radiation.

5. Never accompanied by a thrill.

6. Louder with exercise, fever, or anxiety.

7. Accompanied by no other signs and or symptoms of cardiac disease.

8. Not accompanied by other abnormal cardiac sounds.

Pathological murmurs (those calling referral)

1. All diastolic murmurs.

2. All pansystolic murmurs.

3. All late systolic murmurs.

4. Loud and or accompanied by a thrill,

5. Continuous murmurs (except venous hum).

6. Any murmur heard at the back.

7. Most murmurs transmitted to the neck (except venous hums).

8. Murmurs associated with signs or and symptoms of cardiac disease.

(b) Other signs of cardiac disease


1. Heart sounds—especially loudness and wide or fixed splitting of second sound. or clicks.

2. Central cyanosis.

3. Rapid respiratory rate.

4. Abnormal apex beat or pericardium bulge.

5. Clubbing.

6. Peripheral arterial pulses (radial/ brachial and femoral).

7. Blood-pressure if appropriate cuff is available.

7. Action

Refer to specialised clinic.

1. There are suspicions or doubts as to whether the murmur is pathological.

2. The child has symptoms and or signs of heart disease.

3. The parents are anxious after discussion.

Notify health visitor of referral.

Screening for abnormalities of head circumference.

1. Introduction

Head-circumference measurement may, have an important diagnostic significance in the first few years of life, and is particularly valuable in infants up to one year of age. The routine examination of babies in child-health clinics, in hospital/ or at home should include the measurement of the maximum circumference of the skull, and plotting this on a percentile chart, the reason being that the size of the skull depends in large part on the growth of the cranial contents. By definition 3 per cent of babies will have heads <3rd centile and 3 per cent> than the 97th centile.

2. Aetiologies

The commonest causes of a small head are as follows:

—small baby

—familial feature

—mental subnormality (including congenital diseases)


—abnormal neurological development

but no precise prevalence rates of these causes are available.

The commonest causes for an unusually large head are:

—large baby

—familial feature




—subdural effusion

—cerebral tumour



3. The test

The head circumference can be measured with a paper or plastic tape, as the maximum circumference around the supraorbital ridges and glabella (anteriorly), and that part of the occiput that gives the maximal circumference (pos teriorly). The tape must be pulled tight to compress the hair:

and the measurement is read to the nearest millimetre if the head is abnormally shaped, the serial measurements may best be made by positioning the tape over the points of the forehead and occiput that give the maximal circumference

The head circumference measurement should ideally be taken three times at the same session, averaged, and then plotted on a centile chart.

5. Action

In the face of an abnormal value the obvious potential source of error must be checked before any deductions can be made. Namely: is the method of measurement correct?

If the head circumference after accurate measurement is

A Above the 97th centile,

B Below the 3rd centile

C Cross1ng percentlies.

D In great disparity with the weight centile.


1.Discuss with the parents.

2. Ask the parents about symptoms developmental problems and obstetric or perinatal problems,

3. Check familial history of large / small head-size.

4. Measure the parents head circumference

5. Have the child checked by the clinic doctor.

6. If no other signs or symptoms – measure again in one month.

7. If after one month the head circumference is not growing away from centile lines, treat as normal, if growing away from centiles; refer – with centile chart.

Screening for weight problems

1. Introduction

It can be argued that weight by itself is not a screening test (Hail 1989), as it does not fulfil the criteria of screening’ tests. However routine weighing is carried out, particularly if child health clinics, and so weight is included here for the sake of completeness, Weight-gain is the most widely used clinical measurement of growth in post-natal life, being an index of not only illness and poor nutrition but also in some cases emotional deprivation. Weight should be routinely measured in child-health clinics or at home, and the results plotted on a centile chart so that early diagnosis and intervention can take place.

2. Aetiologies and prevalence’s of poor growth

• Underfeeding (the commonest cause).

• Environmental and socio-psychological deprivation.

• Celiac disease, cystic fibrosis, other malabsorptions.

• Other chronic organic diseases and chronic infections.

• Recognizable congenital syndromes.

• Neuroendocrine or metabolic diseases.

Exact prevalence rates are not available.


It must be remembered that there may be considerable apparent variation of the weight of babies on a day-to-day basis, as a result of:

a)    Whether the baby’s bladder is full or empty.

b)   How recently the baby has been fed.

‘c) The use of different scales.

d) The baby not always being weighed unclothed.

e) If weighed clothed, the amount of clothing worn.

All these factors need to be taken into account.

3. The test

Accurate measurement of weight is required, so certain conditions must be followed:

The scale must be in order.

2. The baby should be naked (whenever possible).

3. After six months of age weight is measured to the last complete 0.1 kg.

4. If the child is restless it may become necessary to weigh him / her held by the mother, and then subtract the mother’s weight.

5. All measurements should be entered on a suitable growth chart.

6. Corrections should be made for gestational age.

4. When to weigh

Accurate measurements of weight should be made up to two years of age, whenever the child attends clinic,in the normal child too frequent weighing is as a rule, undesirable because it is likely to produce anxiety and unnecessarily worry parents, and because minor diseases may temporarily slow the weight progress without any special significance. Obviously where there is concern about a childs weight increased frequency is appropriate.

Screening for height problems

1. Introduction

Measurement of height is an important clinical assessment of skeletal growth and should be performed from two years of age onwards. Results should always be plotted on a percent chart.

2. Aetiologies of short stature



Low birth weight

Note• It has not yet been proved that the measurement of length

is suffictently reliable to provide a good tool for screening purposes. However, if for any reason you have to measure length (that s, if parents ask you to, or where parents are convinced that although weight-gain is satisfactory the child is not growing in length), follow these instructions:

measure the child lying down, with the lower orbital borders in the same vertical plane as the external auditory canal. knees flat. ankles gently pulled to stretch the infant, and feet held vertically. Two observers are needed. Two books are held, one against the top of the head and one against the soles of the feet. The distance between them is measured.

Note on tall children

• Tall children do not generally have organic disease, although they may have some orthopaedic problems. Psychological problems are, however, more important. Some congenital disorders (Soto’s. Beckwiths. Marfans, or Klinefeiters syndromes) may become evident through excessively tall stature. Tall children who come from short families may need investigation. However, for screening purposes. tallness lacks interest. Treatment of tall children is under review.

Screening for cryptorhidism (undescended testis)

1. Introduction

Cryptorchidism is a condition in which one or both testes fail to descend to a normal position well down in the scrotum. it is one of the most common congentital abnormalities in males. The condition is bilateral in about 10 per cent of cases and in the majority of boys it occurs without any association with other maiformations

The incidence of undescended testis varies according to

both the gestational age and the age of the child.

Most testes of boys who have cryptorchidism at birth descend spontaneously within the first year of life. Those testes that are not well down in the scrotum at birth, or testes well down but associated with hydroceles, must be re checked thoughout the whole of the first five years of life.

• born to mothers aged less than twenty years;

• breech delivery; and

• mothers exposed to exogenous oestrogen therapy during the first trimester.

3. The reasons for identifying UDT

The reasons for screening are:

a) Rising infertility rates (low sperm – counts occur in 100 percent of bilateral untreated cases and 75 percent of bilateral treated.

(b) increase in the cancer risk (undescended testes have a risk of developing cancer which is five times greater than that of the average population)

c) Increase in the risk of testicular torsion

(d) Increase in psychological problems (castration complex).

(e) Cosmetic reasons.

(f) Correction of inguinal hernia if associated.

(g) The operation can be performed at around one year.

4. The test

The screening test is to seek for a location of the testis well down in the scrotal sac.

6. Action

1. Boys whose testes are both well down at birth do not need to be followed.

2. Boys whose testes are other than well down in the scrotum at birth, unilaterally or bilaterally—that is, impalpable; or very high in the inguinal pouch or scrotum; or that are high. can be milked down, but retract up again: Follow all of these until five years of age. because some that are in this group and then come down. may subsequently retract up again.

3. All boys whose testis/es have not completely descended by one year should be referred to a paediatric surgeon.

4. Boys whose parents are anxious about their son’s testes and/ or want a further opinion—refer

5. In case of doubt it is preferable to refer.

Source: Essay UK -

About this resource

This coursework was submitted to us by a student in order to help you with your studies.

Search our content:

  • Download this page
  • Print this page
  • Search again

  • Word count:

    This page has approximately words.



    If you use part of this page in your own work, you need to provide a citation, as follows:

    Essay UK, Neonatal. Available from: <> [30-05-20].

    More information:

    If you are the original author of this content and no longer wish to have it published on our website then please click on the link below to request removal: