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When you have completed this unit you should be able to:
It is important that the nursing and medical staff at these clinics and hospitals are able to prevent, diagnose and manage these conditions.
Many of these complications can be prevented with good antenatal and labour care, together with good care of the infant after delivery. Whenever possible, women who are at risk of delivering an infant with complications should be identified before delivery. These women can then be referred for delivery at a level 2 or 3 hospital where special care for the infant is available.
Jaundice is a yellow discolouration of the skin caused by deposits of bilirubin. Jaundice is a clinical sign and not a laboratory measurement.
Red cells in the blood contain a red pigment called haemoglobin, which carries oxygen. Red cells live for a few months only. Therefore, the body is continually forming new red cells in the bone marrow and destroying old red cells in the liver and spleen. The haemoglobin in old red cells is broken down into a yellow pigment called bilirubin. As newborn infants normally have a high haemoglobin concentration, they produce a lot of bilirubin.
Hyperbilirubinaemia is defined as a concentration of total serum bilirubin that is higher than the normal range. Normally the bilirubin concentration in the serum is low at birth, as it has been rapidly removed by the placenta during pregnancy. The bilirubin concentration climbs steadily for the first few days after delivery, before returning to an adult level by 2 weeks.
After birth, bilirubin is carried by the bloodstream to the liver where a special enzyme changes the bilirubin into a water-soluble form. This chemical process is called conjugation. Only when the bilirubin is water soluble (i.e. conjugated) can the liver cells excrete it into the small bile ducts. From here the conjugated bilirubin is carried in the bile to the small intestine, where it is broken down further by bacteria and is excreted in the stool.
During the first weeks of life the enzyme system that conjugates bilirubin in the liver functions slowly. Therefore, the amount of bilirubin increases in the serum and the newborn infant may become jaundiced as the excess bilirubin is deposited in the skin. After a few days the rate of conjugation in the liver increases and much more bilirubin is excreted. As a result, the amount of bilirubin in the serum slowly returns to the normal adult range and any jaundice disappears.
Some of the bilirubin that is conjugated and excreted by the liver in the first weeks of life is often broken down (unconjugated) by another enzyme in the intestine. This bilirubin is then reabsorbed into the bloodstream, adding to the hyperbilirubinaemia. The reabsorption of bilirubin from the intestine is greater in starved and breastfed infants.
It is both difficult and inaccurate to assess the concentration of bilirubin in the serum by clinical examination of the degree of jaundice, especially in an infant with dark skin. It is important to measure the bilirubin concentration of the serum if an infant is very jaundiced. Usually a sample of blood is collected into a capillary tube and spun down to separate the serum from the red cells. The total serum bilirubin (TSB) is then measured with a bilirubinometer and expressed in µmol/l.
The total serum bilirubin (TSB) cannot be estimated accurately by assessing the degree of jaundice in the skin.
This is the mild jaundice that is seen in up to 50% of all healthy term infants during the first 2 weeks of life. Many of these infants are breastfed. These infants are well and do not need any treatment. Physiological jaundice in newborn infants is the result of:
All these factors usually disappear by 2 weeks and the jaundice disappears.
Many healthy infants have mild jaundice.
It is very important to decide whether the jaundice is physiological or abnormal.
It is not uncommon for otherwise healthy breastfed infants to remain jaundiced for more than 2 weeks.
All these conditions may cause an abnormally high TSB and a very jaundiced infant.
Haemolytic disease of the newborn is a condition where antibodies from the mother cross the placenta into the fetal bloodstream. Here these antibodies destroy the fetal red cells (i.e. haemolysis), causing anaemia and an increased production of bilirubin in the fetus and newborn infant. The 2 most important causes of haemolytic disease of the newborn are:
In haemolytic disease of the newborn the blood group of the infant is different to that of the mother as it is inherited from the father.
Red cells have blood group proteins on their surface. A, B, O and D (Rhesus) are the most important blood group proteins. ABO haemolytic disease occurs when the mother is blood group O and her fetus is blood group A or B. For reasons unknown, some group O mothers start producing antibodies to the A or B proteins. These antibodies cross the placenta and cause haemolysis in the fetus by damaging the fetal red cells. With ABO haemolytic disease, the haemolysis is not severe enough to cause anaemia in the fetus but may cause severe jaundice and anaemia in the newborn infant.
The haemolysis results in anaemia (low haemoglobin concentration and low packed cell volume) and jaundice in the newborn infant. An infant with ABO haemolytic disease usually appears normal at delivery but becomes jaundiced within the first 24 hours. The TSB may increase rapidly and reach dangerous levels. Due to the haemolysis, the infant may also become anaemic. ABO haemolytic disease cannot be prevented.
Jaundice on day 1 suggests haemolytic disease.
Rhesus haemolytic disease is a form of haemolytic disease of the newborn, which may occur when the mother is Rhesus negative (she has no D protein on her red cells) and her fetus is Rhesus positive (it has D protein on its red cells). Rhesus haemolytic disease is caused by maternal antibodies to the D (i.e. Rhesus or Rh) protein on the red cells of the fetus. Only if fetal red cells accidentally cross the placenta, and enter the mother’ s bloodstream, will she produce antibodies to the D protein of her fetus. This process is known as sensitisation and may occur in a Rhesus-negative woman during a delivery, miscarriage or placental abruption. Rhesus haemolytic disease is more severe than ABO haemolytic disease. Therefore, the fetus may develop severe anaemia and die before birth. If born alive, the newborn infant rapidly becomes jaundiced and anaemic.
All pregnant women must have their blood group tested at the start of antenatal care. All Rhesus-negative women must be given 100 µg (4 ml) of anti-D immunoglobulin by intramuscular injection within 72 hours of delivery, miscarriage or placental abruption. This prevents sensitisation.
All women must have their blood group identified during pregnancy and all Rhesus-negative mothers must receive anti-D immunoglobulin after delivery.
Jaundice can become dangerous when the concentration of bilirubin in the blood becomes very high. Bilirubin could then enter the brain of the newborn infant and cause bilirubin encephalopathy (also called kernicterus). The risk of bilirubin encephalopathy depends on the severity of the hyperbilirubinaemia. In well, term infants the TSB becomes dangerous and may cause bilirubin encephalopathy above 350 µmol/l while in preterm infants the TSB becomes dangerous above 250 µmol/l.
A high serum concentration of bilirubin can damage the brain.
Bilirubin encephalopathy presents with lethargy, a high-pitched cry and convulsions.
By not allowing the TSB to reach dangerous levels. A number of methods can be used to reduce the TSB:
Early milk feeds help lower the total serum bilirubin.
Phototherapy uses white or blue light to change bilirubin in the skin into a water-soluble form of bilirubin. This water-soluble bilirubin is then carried in the blood to the liver and kidneys, from where it can be excreted without having to be conjugated. Phototherapy is, therefore, able to lower the TSB.
Phototherapy is usually given with a phototherapy unit, which consists of a row of fluorescent tubes. Daylight tubes, white tubes or blue tubes are used. They should be changed after being used for 1000 hours because their effectiveness decreases with time, even if they still appear bright. A perspex (clear plastic) sheet must be placed below the tubes to reduce heat and filter out any ultraviolet light. A perspex sheet also protects the infant if a fluorescent tube breaks or comes loose.
Although exposure to sunlight also lowers the TSB, an infant placed in the sun may rapidly become too hot. Therefore, this form of phototherapy must be used with great caution.
Whenever the TSB is above the normal range and approaches dangerous levels, or if the infant appears very jaundiced. In practice, a simple chart is used to decide when to give phototherapy. If the TSB concentration reaches the phototherapy line, treatment should be started. The phototherapy line is the same as the upper limit of normal for the TSB and increases from birth to day 4 then levels off. Phototherapy is usually started earlier in preterm or sick infants. It is not necessary to give phototherapy to healthy term infants who are jaundiced with a TSB below the phototherapy line. In other words, phototherapy should not be given to well infants with physiological jaundice. It is very difficult to use phototherapy safely if the TSB cannot be measured.
See Figure 5-1 for a phototherapy chart showing the phototherapy line for term infants.
Figure 5-1: Phototherapy chart showing the phototherapy line for term infants.
Prophylactic phototherapy is given when the TSB is still below the phototherapy line, but either the TSB is expected to increase rapidly or the infant is at an increased risk of bilirubin encephalopathy. Therefore, prophylactic phototherapy is started immediately after birth if haemolytic disease of the newborn is suspected or diagnosed. Prophylactic phototherapy is often given to preterm infants when their TSB gets near the phototherapy line.
It is difficult to give phototherapy safely if the TSB cannot be measured.
Continue phototherapy until the TSB has been under the phototherapy line for 24 hours. Sometimes the TSB rises above the line again after the phototherapy has been stopped. If so, the phototherapy should be restarted.
The total serum bilirubin should be measured in all infants receiving phototherapy.
If the TSB cannot be measured at the level 1 clinic or hospital, a heparinized capillary tube of blood should be sealed at both ends with plasticine and placed in a box to keep light away. It must be sent to the nearest laboratory, which should phone the result to the clinic or hospital as soon as it is available. While waiting for the result, phototherapy should be started.
These infants should be discussed with the staff of the referral hospital before transfer.
Because they have an immature immune system and are exposed to infectious organisms during pregnancy, delivery and in the nursery. The risk of infection in the newborn infant is much higher than in older children or adults. Infection is important as it is one of the commonest causes of death in infants during the first few months of life.
Infection is a common cause of death in young infants.
There are many simple ways in which infections can be prevented in the newborn infant:
Breast milk protects against infections.
It is not necessary to restrict visits of parents and family in the nursery provided that strict hand washing and hand spraying is enforced. There is no need for visitors to wear masks or gowns. If possible, family and staff with coughs, colds and ’flu should not handle infants. Herpes infection (fever blisters) can cause a very serious infection. Infants should not be kissed.
Conjunctivitis presents with:
The degree of conjunctivitis can be divided clinically into mild, moderate and severe:
Conjunctivitis is usually mild. It is difficult to clinically identify the organism causing conjunctivitis, although severe conjunctivitis is usually caused by Gonococcus from the mother’s cervix and vagina. Therefore, the management depends on the severity rather than the cause.
Gonococcus causes severe conjunctivitis which may result in blindness.
A healthy umbilical cord stump is white and soft at delivery. With good cord care it becomes dark brown and dehydrated within a few days, and at no stage does it smell offensive or produce pus. The aim of good cord care is to dry the cord and keep it clean.
Infection of the umbilical cord (omphalitis) presents with:
The commonest site of infection is at the base where the cord meets the skin. When the infection is localised to the cord only, there is no oedema of the skin around the base of the cord and the infant is generally well. Umbilical cord infection may spread to the anterior abdominal wall from where it may cause a peritonitis or septicaemia. Signs that the infection of the umbilical cord has extended to the abdominal wall are:
Cellulitis, peritonitis and septicaemia are serious infections and the infant may die if not treated immediately with intramuscular or intravenous antibiotics. Infection of the umbilical cord may also cause tetanus in the newborn infant.
With good preventative cord care, infection of the umbilical cord should not occur. Prevention consists of routine applications of alcohol (surgical spirits) or chlorhexidine solution to the cord every time the nappy is changed until it is dehydrated. Antibiotic powder is not used. Do not put aspirin or other home remedies on the cord. Never cover the cord with the nappy or a bandage as this keeps it moist.
If the infection is localised to the umbilical cord, and there are no signs of cellulitis, peritonitis, septicaemia or tetanus, then treatment consists simply of repeatedly cleaning the cord with surgical spirits to clear the infection and hasten dehydration. Neither local nor systemic antibiotics are needed. Special attention must be paid to the folds around the base of the cord, which often remain moist. Within 24 hours the infection should have cleared. Keep a careful watch for signs that the infection may have spread beyond the umbilicus.
Tetanus in the newborn infant (tetanus neonatorum) is caused by bacteria, which infect dead tissues such as the umbilical cord. Tetanus bacteria usually occurs in soil and faeces, which may be placed on the cord or other wounds as a traditional practice. They produce a powerful toxin that affects the nervous system.
Tetanus presents with:
Tetanus can be prevented by:
The emergency treatment of tetanus consists of:
The 2 commonest forms of skin infection in the newborn infant are:
A sweat rash, due to excessive sweating, may look like an infection. It presents as small clear blisters on the forehead or a fine red rash on the neck and trunk. Treat by washing the infant to remove the sweat and prevent overheating.
If you pay strict attention to hand washing and spraying, and do not routinely wash off vernix, then skin infection should not be a problem in the nursery.
Oral thrush is caused by a fungus (Candida or Monilia). It presents as a patchy white coating on the tongue and mucus membrane of the mouth. Unlike a deposit of milk curds sometimes seen after a feed, thrush cannot easily be wiped away. Mild thrush is very common, especially in breastfed infants and usually requires no treatment. In contrast, with severe thrush the tongue and mucous membrane are red and covered with a thick white layer of fungus. The infant feeds poorly due to a painful mouth. The infant appears miserable and may lose weight or even become dehydrated.
Severe thrush should be treated with 1 ml mycostatin drops (Nystatin) into the mouth after each feed. Mycostatin ointment can also be used and should be wiped onto the oral mucus membrane with a swab or clean finger. Treatment should be continued for a week. Gentian violet can be used on the thrush if mycostatin is not available. In a breastfed infant the source is usually monilial infection of the mother’s nipples. Mycostatin ointment should be smeared on the nipple and areola after each feed. If the mother has a monilial vaginal discharge, this should be treated with mycostatin vaginal cream to reduce the amount of Candida on the mother’s skin. In bottle-fed infants, the bottles and teats must be boiled after the feed. Disinfectant solutions such as Milton and Jik are very useful to prevent bacterial contamination of bottles, but may not kill Candida. Dummies should be boiled or thrown away.
The clinical signs of septicaemia are often non-specific, making the early diagnosis of septicaemia difficult. The common clinical signs are:
The infant may also have signs of pneumonia, meningitis or necrotising enterocolitis.
Management of septicaemia consists of:
An infant born with congenital syphilis may have one or more of the following signs:
Some infants that have recently acquired congenital syphilis may have no clinical signs yet. If untreated, most of these asymptomatic infants will develop clinical signs of syphilis within a few months. Infants with congenital syphilis will have a positive VDRL or RPR test.
The method of treatment depends on whether the infant has clinical signs of congenital syphilis or not:
If an HIV positive women does not receive antiretroviral (ARV) treatment during pregnancy, labour and during breast feeding, and the infant does not receive prophylactic antiretroviral medication after birth, the risk of HIV infecting her infant is approximately 25%. However if ARVs are used correctly this risk is reduced to less than 2%. The current ARV regimen for women in South Africa is daily fixed dose combination (FDC) pill of TDF (tenofavir), FTC (emtricitabine ) and efavirenz (EFV) during pregnancy and labour and then for life.
All HIV exposed infants should be given an oral dose of nevirapine (NVP) as soon as possible after delivery and then a daily dose until the age of 6 weeks (post exposure prophylaxis). With breastfed infants the NVP should be continued until two weeks after the last breastfeed. All HIV exposed infants should have a PCR test at birth, 10 weeks and six weeks after the last breastfeed.
At birth, 10 weeks of age and two weeks after the last breastfeed a PCR test should be done on all HIV exposed infants to determine whether the infant has been infected with HIV or not. If the test is negative the infant has not been infected and should received routine primary care.
All HIV exposed infants should be given a daily dose of nevirapine for six weeks after delivery.
Most term infants will need 1.5 ml NVP from birth to six weeks.
|Birth weight||Daily dosage||Quantity|
|NVP syrup 10 mg/ml||Less than 2.0 kg||First 2 weeks: 2 mg/kg||0.2 ml/kg|
|Next 4 weeks: 4 mg/kg||0.4 ml/kg|
|2.0 – 2.5 kg||Birth to 6 weeks: 10 mg||1.0 ml|
|More than 2.5 kg||Birth to 6 weeks: 15 mg||1.5 ml|
If the PCR test is positive the infant has been infected with HIV and must have further management which will include lifelong ARV treatment. These infants must be cared for at a clinic or hospital which can provide the national protocol of HIV management.
A cephalhaematoma is a collection of blood under the periosteum of the parietal bone of the skull. It is common, appears within hours of delivery as a soft swelling on the side of the head, and may be on one or both sides. A cephalhaematoma is caused by damage to capillaries under the periosteum and, therefore, never extends beyond the edges of the bone. Cephalhaematomas are usually small and need no treatment. The absorption of blood may cause jaundice, however, which may require treatment by phototherapy. It can take up to 3 months before the cephalhaematoma disappears. Never aspirate a cephalhaematoma as it may result in further bleeding or infection.
Never aspirate or drain a cephalhaematoma.
In contrast, a subaponeurotic haemorrhage is a collection of blood under the scalp. Fortunately a subaponeurotic haemorrhage is not common as it rapidly results in shock due to blood loss.
A brachial plexus injury (or Erb’s palsy) is caused by excessive pulling on the head and neck during delivery. The infant is usually large and born at term with difficulty delivering the shoulders. Brachial palsy may also complicate a poorly managed breech delivery. By over-stretching the neck, the brachial plexus of nerves in the infant’s neck is damaged.
Immediately after birth it is noticed that the infant does not move one arm due to weakness at the shoulder and elbow. The arm remains fully extended and held beside the body. The infant is unable to flex that arm at the elbow or lift the arm off the bed. Movement of the hand and fingers is normal, however. The infant also has a markedly asymmetrical Moro reflex. Unless there is an associated fracture, there is no tenderness, pain or swelling of the arm.
Usually the weakness is much better by a week and full movement and power returns within a month. If the weakness is not much improved by a week, refer the infant to a level 2 or 3 hospital for assessment. Keeping the arm above the head will not help recovery.
A facial palsy presenting with weakness of one side of the face after delivery is not common and usually recovers within a few days.
Bruising is common after difficult deliveries, especially breech delivery in a preterm infant. The bruise is due to bleeding into the skin. A tight umbilical cord around the neck commonly causes severe congestion and bruising of the face. The bruise fades after a week or two and needs no treatment. The absorbed blood may cause jaundice, requiring phototherapy.
Rarely, fractures of the clavicle (collar bone), humerus or even femur occur after a very difficult delivery. These fractures usually heal well without splinting. Paracetamol (Panado syrup 2.5 ml) should be given for pain relief in all fractures.
Bleeding from the cut umbilical cord due to a slipped cord clamp or cord tie. Therefore, it is very important to make sure that the cord is clamped or tied correctly, or the infant may bleed severely.
Haemorrhagic disease of the newborn is bleeding due to a lack of vitamin K1, which is needed by the infant to produce clotting factors in the liver. During pregnancy the fetus does not get much vitamin K1 from the mother and there is not much vitamin K1 in breast milk.
Infants with haemorrhagic disease of the newborn usually bleed from their umbilical cord, vomit blood or have blood in their stools during the first week of life. If severe, the infant can bleed to death. Any infant presenting with bleeding must be given 1 mg of Konakion (vitamin K1) and urgently referred to a level 2 or 3 unit. If very pale and shocked, the infant must first be resuscitated and given intravenous fluid.
By giving all infants 1 mg (0.1 ml) of Konakion by intramuscular injection after delivery. This is best given into the lateral thigh (NOT into the buttock).
All babies must be given intramuscular Konakion after delivery.
Oral Konakion should not be used, as it cannot be relied on to prevent haemorrhagic disease unless it is given repeatedly.
Purpura (or petechiae) are small bleeds under the skin presenting as pink or blue spots. Purpura usually only occurs over part of the body and is caused by pulling and squeezing of the arms or legs during a difficult delivery. It disappears after a few days. If purpura occurs over the whole body there is probably some abnormality with the infant’s platelets. These infants must be urgently referred to a level 2 or 3 hospital for investigation and treatment. Do not confuse purpura with the blue patches (Mongolian spots) commonly seen over the back.
A convulsion (fit) may present as:
It is often very difficult to recognise a convulsion in a newborn infant as infants usually do not have a grand mal fit (generalised extension followed by jerking movements) as seen in older children and adults.
Jitteriness and the movements normal infants make while asleep must not be confused with convulsions. Unlike convulsions, jitteriness can be stimulated by handling the infant. In addition, jitteriness can be stopped by holding that limb.
The important causes of convulsions in the newborn infant are:
Convulsions in the first few days of life are usually due to hypoxia during labour.
A well, breastfed term infant develops jaundice on day 3. The TSB (total serum bilirubin) is 120 µmol/l, which falls into the normal range for day 3. Both the mother and infant are blood group O positive.
This infant probably has physiological jaundice caused by slow bilirubin conjugation by the liver and increased bilirubin reabsorption by the intestines.
Because both the mother and infant have the same ABO and Rhesus blood groups.
No, this infant does not have hyperbilirubinaemia because the TSB falls within the normal range for day 3.
The infant should be managed as for a healthy, normal infant except that the TSB should be repeated daily until it starts to fall.
No. There is no reason for phototherapy.
No, she should continue to breastfeed. Although breastfeeding may result in a slightly higher TSB, it is not necessary to stop breastfeeding.
The mother delivers a 2000 g infant at home. On day 2 the infant develops bilateral purulent conjunctivitis. When he is brought to the local clinic his eyelids are swollen. Otherwise the infant is well with no other abnormal signs. However, it is noticed that the mother was VDRL positive during her pregnancy and was not treated.
Gonococcus. This is the commonest cause of severe conjunctivitis. The infant was probably infected during delivery.
By placing chloromycetin ointment into the infant’s eyes after delivery.
Because the eyelids are swollen and the eyes are filled with pus.
The cornea may become soft and perforate, causing blindness.
The eyes must be washed out with saline or water. They should then be washed out or irrigated repeatedly until the pus stops forming. In addition, procaine penicillin 100 000 units must be given by intramuscular injection daily for 3 days. Only when the eyes are clean and the first dose of penicillin has been given should the infant be referred to hospital for further treatment.
Because it indicates that she probably has syphilis. If the mother has not been fully treated, the infant must be treated as he may have asymptomatic syphilis infection.
If the infant has no clinical signs of syphilis the treatment is a single intramuscular dose of 50 000 units/kg benzathine penicillin. If the infant had clinical signs of syphilis the treatment would be procaine penicillin 50 000 units/kg IM daily for 10 days.
An infant weighing 5000 g is born in a level 2 hospital. The shoulders are delivered with great difficulty. After birth it is noticed that the infant does not move her right arm much and has an asymmetrical Moro reflex.
She probably has a brachial plexus injury (Erb’s palsy) caused by excessive downward traction (pulling) on the neck during the difficult delivery of the shoulders.
The infant will have weakness of the shoulder and elbow and will be unable to lift her arm off the bed or flex the elbow against gravity. Movement and power in the hand will be normal. Unless there is a fracture, there should be no tenderness.
Usually the weakness is much improved by a week.
If the weakness is not much better after a week, the infant must be referred to a level 2 or 3 hospital for further management.
A preterm infant weighing 1500 g is born at home. The infant is transferred to hospital but the staff forget to give Konakion. On day 5 the infant passes a lot of fresh blood in the stool, has a small dark brown vomit and appears pale.
The infant probably has haemorrhagic disease of the newborn.
Yes. Haemorrhagic disease of the newborn should not be seen if Konakion is given routinely to all infants.
Vitamin K1. This must be given to all infants at birth by intramuscular injection into the thigh.
Give 1 mg Konakion immediately. Start an intravenous infusion if the infant appears pale and shocked. Discuss the infant with the staff at the referral hospital and transfer the infant as soon as possible.