Newborn Care was written for healthcare workers providing special care for newborn infants in level 2 hospitals. It covers: resuscitation at birth, assessing infant size and gestational age, routine care and feeding of both normal and high-risk infants, the prevention, diagnosis and management of hypothermia, hypoglycaemia, jaundice, respiratory distress, infection, trauma, bleeding and congenital abnormalities, communication with parents
Hypothermia is a significant problem in neonates that can lead to increased mortality and morbidity. It is caused by situations that lead to excessive heat loss or poor ability to produce heat in babies. These include cold environments, wet skin, procedures like bathing, and low birth weight. Newborns are prone to hypothermia due to their large surface area and limited ability to generate heat. Prevention focuses on keeping babies warm through immediate drying and skin-to-skin contact with the mother. Treatment involves gradually rewarming the baby and minimizing further heat loss. Healthcare providers must be alert to the risks and take steps to maintain the baby's temperature within a normal range.
This document discusses transient tachypnea of the newborn (TTN). TTN is a common condition caused by a delay in clearing fetal lung fluid after birth. It presents with respiratory distress and affects up to 15% of preterm infants. Risk factors include cesarean delivery, prematurity, and gestational diabetes. Diagnosis is based on clinical presentation, physical exam, and chest x-ray findings showing diffuse haziness. Treatment involves respiratory support and monitoring as symptoms typically resolve within 3 days. Medications are not routinely used or recommended for TTN management.
Croup is a common respiratory illness in young children caused by viruses such as parainfluenza. It causes barking cough, hoarseness, and stridor. Symptoms typically worsen at night. Diagnosis is clinical based on symptoms and appearance of the steeple sign on chest x-ray. Treatment involves corticosteroids which reduce symptoms, and nebulized epinephrine for more severe cases. Most children recover without complications, though a small percentage require hospitalization for respiratory support.
The document discusses neonatal hypoglycemia, including its definition, symptoms, risk factors, treatment, and monitoring. Some key points:
- Neonatal hypoglycemia is defined as a blood glucose level below certain thresholds in the first 24 hours and thereafter. It is a common problem in newborns.
- Babies at higher risk include preterms, those of diabetic mothers, or experiencing other stresses. Symptoms can be nonspecific.
- Treatment involves glucose administration via IV bolus or infusion to raise blood glucose to the normal range. Frequent monitoring is needed until levels stabilize.
- Persistent or resistant hypoglycemia may require additional drugs or referral to a specialist to investigate underlying
respiratory difficulty commonly in a preterm neonate and is due to deficiency of pulmonary surfactant. It was formerly known as Hyaline Membrane Disease (HMD).
presented by Dr. Taher
The document provides information on ascites in children, including causes, pathophysiology, clinical presentation, investigations, and management. The most common causes of ascites in children are hepatic and renal disease, though it can also be caused by cardiac disease, trauma, infection, or neoplasia. Diagnostic evaluation involves physical exam, imaging like ultrasound or CT scan, and paracentesis with ascitic fluid analysis. Management depends on the underlying cause but may include diuretics, salt restriction, liver support therapies, or treatment of the primary disease. Complications can include respiratory distress, hernias, infections like spontaneous bacterial peritonitis.
Bronchiolitis is an inflammatory disease of the small airways caused primarily by Respiratory Syncytial Virus (RSV) in infants under 1 year old. It leads to obstruction of the small airways due to inflammation, mucus production, and edema. Clinically, infants present with rhinorrhea, cough, tachypnea, wheezing and respiratory distress. Chest X-ray may show hyperinflated lungs. Management is supportive with oxygen, hydration and sometimes bronchodilators. Most infants recover within 2 weeks but some may develop long-term wheezing.
Neonatal sepsis occurs when bacteria enter the bloodstream of infants less than 90 days old. It can cause overwhelming infection or spread to organs like the lungs (pneumonia) or meningitis. Common causes are E. coli, listeria, and certain streptococcus bacteria. Risk factors include preterm birth, maternal infection, and hospitalization after birth. Symptoms are non-specific but include temperature changes, breathing issues, poor feeding, and lethargy. Diagnosis involves blood, urine, and CSF tests and treatment is with antibiotics like ampicillin and gentamicin alongside supportive care. Outcomes can vary from full recovery to neurological or respiratory problems, especially in preterm infants.
Hypothermia is a significant problem in neonates that can lead to increased mortality and morbidity. It is caused by situations that lead to excessive heat loss or poor ability to produce heat in babies. These include cold environments, wet skin, procedures like bathing, and low birth weight. Newborns are prone to hypothermia due to their large surface area and limited ability to generate heat. Prevention focuses on keeping babies warm through immediate drying and skin-to-skin contact with the mother. Treatment involves gradually rewarming the baby and minimizing further heat loss. Healthcare providers must be alert to the risks and take steps to maintain the baby's temperature within a normal range.
This document discusses transient tachypnea of the newborn (TTN). TTN is a common condition caused by a delay in clearing fetal lung fluid after birth. It presents with respiratory distress and affects up to 15% of preterm infants. Risk factors include cesarean delivery, prematurity, and gestational diabetes. Diagnosis is based on clinical presentation, physical exam, and chest x-ray findings showing diffuse haziness. Treatment involves respiratory support and monitoring as symptoms typically resolve within 3 days. Medications are not routinely used or recommended for TTN management.
Croup is a common respiratory illness in young children caused by viruses such as parainfluenza. It causes barking cough, hoarseness, and stridor. Symptoms typically worsen at night. Diagnosis is clinical based on symptoms and appearance of the steeple sign on chest x-ray. Treatment involves corticosteroids which reduce symptoms, and nebulized epinephrine for more severe cases. Most children recover without complications, though a small percentage require hospitalization for respiratory support.
The document discusses neonatal hypoglycemia, including its definition, symptoms, risk factors, treatment, and monitoring. Some key points:
- Neonatal hypoglycemia is defined as a blood glucose level below certain thresholds in the first 24 hours and thereafter. It is a common problem in newborns.
- Babies at higher risk include preterms, those of diabetic mothers, or experiencing other stresses. Symptoms can be nonspecific.
- Treatment involves glucose administration via IV bolus or infusion to raise blood glucose to the normal range. Frequent monitoring is needed until levels stabilize.
- Persistent or resistant hypoglycemia may require additional drugs or referral to a specialist to investigate underlying
respiratory difficulty commonly in a preterm neonate and is due to deficiency of pulmonary surfactant. It was formerly known as Hyaline Membrane Disease (HMD).
presented by Dr. Taher
The document provides information on ascites in children, including causes, pathophysiology, clinical presentation, investigations, and management. The most common causes of ascites in children are hepatic and renal disease, though it can also be caused by cardiac disease, trauma, infection, or neoplasia. Diagnostic evaluation involves physical exam, imaging like ultrasound or CT scan, and paracentesis with ascitic fluid analysis. Management depends on the underlying cause but may include diuretics, salt restriction, liver support therapies, or treatment of the primary disease. Complications can include respiratory distress, hernias, infections like spontaneous bacterial peritonitis.
Bronchiolitis is an inflammatory disease of the small airways caused primarily by Respiratory Syncytial Virus (RSV) in infants under 1 year old. It leads to obstruction of the small airways due to inflammation, mucus production, and edema. Clinically, infants present with rhinorrhea, cough, tachypnea, wheezing and respiratory distress. Chest X-ray may show hyperinflated lungs. Management is supportive with oxygen, hydration and sometimes bronchodilators. Most infants recover within 2 weeks but some may develop long-term wheezing.
Neonatal sepsis occurs when bacteria enter the bloodstream of infants less than 90 days old. It can cause overwhelming infection or spread to organs like the lungs (pneumonia) or meningitis. Common causes are E. coli, listeria, and certain streptococcus bacteria. Risk factors include preterm birth, maternal infection, and hospitalization after birth. Symptoms are non-specific but include temperature changes, breathing issues, poor feeding, and lethargy. Diagnosis involves blood, urine, and CSF tests and treatment is with antibiotics like ampicillin and gentamicin alongside supportive care. Outcomes can vary from full recovery to neurological or respiratory problems, especially in preterm infants.
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This neonatal case presentation involves a 16 day old infant admitted to the NICU with jaundice since birth and vomiting for 1 day. Investigations revealed severe anemia, indirect hyperbilirubinemia, increased reticulocyte count, and elevated LDH. The infant received a PRBC transfusion and was discharged with improved Hb. The clinical picture is suggestive of hemolytic anemia, possibly due to fetomaternal hemorrhage given the maternal history of blood transfusions in the second trimester.
This document discusses pneumonia in children. It provides definitions, epidemiology, risk factors, classification, etiology, clinical presentation, investigations, treatment and prevention of pneumonia. Some key points:
- Pneumonia is the leading cause of death among children under 5 globally, accounting for 16% of deaths. It occurs most frequently in developing countries.
- Risk factors include malnutrition, low birth weight, lack of breastfeeding, lack of immunization, indoor air pollution, parental smoking, and zinc deficiency.
- Clinical features depend on the causative agent. Bacterial pneumonia presents with high fever and chest pain while viral pneumonia shows low grade fever and respiratory distress.
- Investigations include chest X-ray
1. Acute glomerulonephritis is a common kidney disease in children that is often preceded by a streptococcal infection. It causes blood in the urine and can lead to reduced urine output, swelling, and high blood pressure.
2. The disease is an immune-mediated inflammatory response in the glomeruli of the kidneys caused by antigen-antibody complexes depositing in the glomerular capillaries, resulting in kidney damage.
3. Treatment focuses on controlling symptoms like blood pressure and swelling through bed rest, fluid management, and medications. Antibiotics may be given if caused by a streptococcal infection.
This document discusses Pyloric Stenosis and provides details about its causes, symptoms, diagnosis, and treatment. It occurs in infants between 2 to 8 weeks of age due to hypertrophy and hyperplasia of the pylorus muscles. Symptoms include projectile vomiting and failure to gain weight. Diagnosis is confirmed by barium meal x-ray. Treatment involves rehydration followed by pyloromyotomy surgery to open the stomach outlet. The document also briefly discusses Hirschsprung's disease, another pediatric gastrointestinal condition caused by the absence of ganglionic cells in the intestine.
Fever is a common medical symptom defined as a temperature above the normal range of 36.8-37.2°C or 98.2-98.6°F. It is not an illness itself but rather a sign that the body's immune system is fighting infection. There are various methods for measuring a person's temperature including oral, armpit, ear, and rectal thermometers. Treatment of fever involves medication such as acetaminophen to reduce temperature as well as other supportive measures like light clothing and increased fluids. Repeated or high fever may require medical evaluation to check for underlying infection.
Meconium aspiration syndrome (MAS) is a respiratory distress in infants born through meconium stained amniotic fluid. It occurs in 5% of infants delivered through meconium stained fluid and is caused by mechanical obstruction and chemical pneumonitis from inhaled meconium. Clinical features include respiratory distress, cyanosis, and chest retractions. Diagnosis is confirmed by chest x-ray showing infiltrates and management involves ventilatory support, surfactant therapy, inhaled nitric oxide, and potentially extracorporeal membrane oxygenation. With aggressive treatment, mortality from MAS has decreased to less than 5%.
Urinary tract infections are common in children, especially girls. The most common cause is Escherichia coli bacteria spreading from the intestines. Symptoms vary from mild cystitis to severe pyelonephritis. Diagnosis involves urinalysis and urine culture. Treatment depends on severity but commonly involves antibiotics like trimethoprim-sulfamethoxazole. Imaging with ultrasound is recommended for the first UTI in infants and children under 3, or those with fever or systemic illness, to check for anatomical abnormalities.
This document describes a case of omphalitis, an infection of the umbilical stump, in a 7-day-old male infant. The infant presented with fever, yellowish umbilical discharge, and hypoactivity. Laboratory tests showed elevated white blood cell count and C-reactive protein. The infant was diagnosed with omphalitis and sepsis and started on intravenous antibiotics and supportive care. Omphalitis is a potentially serious infection in neonates that requires prompt treatment with antibiotics and sometimes surgery.
This document summarizes meningitis in children, including the definition, causes, signs and symptoms, diagnosis, treatment, and prevention. Meningitis is an inflammation of the membranes surrounding the brain and spinal cord. It most commonly affects infants and children under 5 years old. Bacteria such as pneumococcus, meningococcus, and H. influenzae are common causes. Signs include fever, headache, neck stiffness, and altered mental status. Diagnosis involves lumbar puncture and culture of spinal fluid. Treatment involves antibiotics and supportive care. Vaccines can help prevent certain bacterial types. Complications may include neurological deficits if not treated promptly.
Clinically, more term babies suffered from hypoxic ischemic encephalopathy (HIE) than premature babies. However, pathologically, more premature babies suffered from HIE than term babies. HIE manifests clinically as symptoms of consciousness changes that can be excitatory like seizures or depressing like coma. Treatment of HIE focuses on monitoring, controlling seizures, maintaining circulation and glucose levels, with therapies like hypothermia and investigates like amplitude integrated EEG shown to improve outcomes. The prognosis depends on the severity of brain damage and treatment, with mild cases often having a full recovery but severe cases having a high risk of mortality or neurological sequele like cerebral palsy.
Acute kidney injury (AKI), formerly called acute renal failure, is a sudden deterioration of renal function that results in the buildup of waste products and fluid overload. It ranges from a minor increase in creatinine to complete kidney failure. Causes include decreased blood flow to the kidneys (prerenal), direct kidney damage (intrarenal), or urinary tract obstruction (postrenal). Symptoms include decreased urine output, retention of waste products, fluid overload, and electrolyte imbalances. Treatment focuses on fluid management, treating the underlying cause, and dialysis in severe cases. Chronic kidney disease (CKD) is the gradual loss of kidney function over time defined as kidney damage and/or decreased G
Approach to a child with HepatosplenomegalySunil Agrawal
This document discusses hepatosplenomegaly, or the enlargement of the liver and spleen. It begins with an introduction and overview of hepatomegaly and splenomegaly. It then covers the various causes of hepatosplenomegaly including infections, hematological disorders, vascular congestion, tumors and infiltrations, storage disorders, and miscellaneous causes. The document provides details on evaluating a patient's history, physical examination findings, investigations, and treatment strategies for hepatosplenomegaly in both children and neonates. It concludes with references for further information.
Neonatal sepsis is a clinical syndrome characterized by signs and symptoms of infection in the first month of life. It can involve sepsis, meningitis, pneumonia and other infections. The document discusses the definition, classification, risk factors, clinical features, investigations and management of neonatal sepsis. Key points include that sepsis is a leading cause of neonatal mortality, the importance of sepsis screening and blood cultures, and that initial empirical antibiotic therapy typically involves ampicillin and an aminoglycoside.
This presentation focuses on Acute Bacterial Meningitis.
Viral and fungal cause is mentioned but focus is on bacterial meningitis in Pediatrics Patient.
Feel free to correct if there is any error.
Refer to other reference books for clarity.
This document discusses malaria in children, including its classification, epidemiology, etiology, clinical features, complications, management, prognosis and prevention. It provides details on the life cycle and transmission of the plasmodium parasite. For diagnosis, it recommends looking for malarial parasites in blood smears or using rapid diagnostic tests. It describes the clinical features of malaria as fever, often alternating daily or every two days. Complications can include anemia, jaundice and cerebral malaria. Management involves antipyretics, hydration, nutrition and antimalarial drugs depending on the plasmodium species and local resistance patterns. Prevention methods are use of mosquito nets and chemoprophylaxis. The document also briefly discusses visceral
A preterm newborn developed respiratory distress soon after birth, with signs including grunting and cyanosis. Evaluation found respiratory distress syndrome (RDS). The baby was treated with nasal CPAP, surfactant, and mechanical ventilation. RDS is caused by surfactant deficiency in premature infants, resulting in alveolar collapse and impaired gas exchange. Management includes respiratory support, surfactant replacement therapy, and care to prevent complications.
This document discusses prematurity and its complications. It defines prematurity as infants born before 37 weeks gestation according to the WHO. Prematurity is classified based on gestational age as extremely, very, or moderate to late preterm. It can also be classified based on birth weight as low, very low, or extremely low. Risk factors include socioeconomic status, previous prematurity, and maternal health conditions. Causes include fetal, uterine, maternal, and iatrogenic factors. Clinical presentation includes weak reflexes and poor muscle tone. Complications involve respiratory, cardiovascular, gastrointestinal, metabolic, central nervous system, renal, and infectious issues. Long term complications may include developmental delays. Care after birth focuses on stabilization, monitoring,
This document discusses neonatal jaundice (hyperbilirubinemia) in infants. It covers the definition, causes, types (physiological vs pathological), investigations, management including phototherapy and exchange transfusion, and prevention of kernicterus. Key points include:
- Jaundice is caused by high bilirubin levels which cause yellowing of the skin and eyes. Bilirubin is produced from the breakdown of red blood cells.
- Physiological jaundice appears after 24-72 hours and is common, while pathological jaundice appears within 24 hours and requires treatment.
- Management involves phototherapy to reduce bilirubin levels or exchange transfusion for severe
Management of child with neonatal jaundiceNEHA MALIK
Newborn jaundice is a yellowing of a baby's skin and eyes. Newborn jaundice is very common and can occur when babies have a high level of bilirubin, a yellow pigment produced during normal breakdown of red blood cells.
follow me on my YouTube channel :- medic o mania
Neonatal jaundice (hyperbilirubinemia) by Rajiv MavachiRajiv Mavachi
Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This neonatal case presentation involves a 16 day old infant admitted to the NICU with jaundice since birth and vomiting for 1 day. Investigations revealed severe anemia, indirect hyperbilirubinemia, increased reticulocyte count, and elevated LDH. The infant received a PRBC transfusion and was discharged with improved Hb. The clinical picture is suggestive of hemolytic anemia, possibly due to fetomaternal hemorrhage given the maternal history of blood transfusions in the second trimester.
This document discusses pneumonia in children. It provides definitions, epidemiology, risk factors, classification, etiology, clinical presentation, investigations, treatment and prevention of pneumonia. Some key points:
- Pneumonia is the leading cause of death among children under 5 globally, accounting for 16% of deaths. It occurs most frequently in developing countries.
- Risk factors include malnutrition, low birth weight, lack of breastfeeding, lack of immunization, indoor air pollution, parental smoking, and zinc deficiency.
- Clinical features depend on the causative agent. Bacterial pneumonia presents with high fever and chest pain while viral pneumonia shows low grade fever and respiratory distress.
- Investigations include chest X-ray
1. Acute glomerulonephritis is a common kidney disease in children that is often preceded by a streptococcal infection. It causes blood in the urine and can lead to reduced urine output, swelling, and high blood pressure.
2. The disease is an immune-mediated inflammatory response in the glomeruli of the kidneys caused by antigen-antibody complexes depositing in the glomerular capillaries, resulting in kidney damage.
3. Treatment focuses on controlling symptoms like blood pressure and swelling through bed rest, fluid management, and medications. Antibiotics may be given if caused by a streptococcal infection.
This document discusses Pyloric Stenosis and provides details about its causes, symptoms, diagnosis, and treatment. It occurs in infants between 2 to 8 weeks of age due to hypertrophy and hyperplasia of the pylorus muscles. Symptoms include projectile vomiting and failure to gain weight. Diagnosis is confirmed by barium meal x-ray. Treatment involves rehydration followed by pyloromyotomy surgery to open the stomach outlet. The document also briefly discusses Hirschsprung's disease, another pediatric gastrointestinal condition caused by the absence of ganglionic cells in the intestine.
Fever is a common medical symptom defined as a temperature above the normal range of 36.8-37.2°C or 98.2-98.6°F. It is not an illness itself but rather a sign that the body's immune system is fighting infection. There are various methods for measuring a person's temperature including oral, armpit, ear, and rectal thermometers. Treatment of fever involves medication such as acetaminophen to reduce temperature as well as other supportive measures like light clothing and increased fluids. Repeated or high fever may require medical evaluation to check for underlying infection.
Meconium aspiration syndrome (MAS) is a respiratory distress in infants born through meconium stained amniotic fluid. It occurs in 5% of infants delivered through meconium stained fluid and is caused by mechanical obstruction and chemical pneumonitis from inhaled meconium. Clinical features include respiratory distress, cyanosis, and chest retractions. Diagnosis is confirmed by chest x-ray showing infiltrates and management involves ventilatory support, surfactant therapy, inhaled nitric oxide, and potentially extracorporeal membrane oxygenation. With aggressive treatment, mortality from MAS has decreased to less than 5%.
Urinary tract infections are common in children, especially girls. The most common cause is Escherichia coli bacteria spreading from the intestines. Symptoms vary from mild cystitis to severe pyelonephritis. Diagnosis involves urinalysis and urine culture. Treatment depends on severity but commonly involves antibiotics like trimethoprim-sulfamethoxazole. Imaging with ultrasound is recommended for the first UTI in infants and children under 3, or those with fever or systemic illness, to check for anatomical abnormalities.
This document describes a case of omphalitis, an infection of the umbilical stump, in a 7-day-old male infant. The infant presented with fever, yellowish umbilical discharge, and hypoactivity. Laboratory tests showed elevated white blood cell count and C-reactive protein. The infant was diagnosed with omphalitis and sepsis and started on intravenous antibiotics and supportive care. Omphalitis is a potentially serious infection in neonates that requires prompt treatment with antibiotics and sometimes surgery.
This document summarizes meningitis in children, including the definition, causes, signs and symptoms, diagnosis, treatment, and prevention. Meningitis is an inflammation of the membranes surrounding the brain and spinal cord. It most commonly affects infants and children under 5 years old. Bacteria such as pneumococcus, meningococcus, and H. influenzae are common causes. Signs include fever, headache, neck stiffness, and altered mental status. Diagnosis involves lumbar puncture and culture of spinal fluid. Treatment involves antibiotics and supportive care. Vaccines can help prevent certain bacterial types. Complications may include neurological deficits if not treated promptly.
Clinically, more term babies suffered from hypoxic ischemic encephalopathy (HIE) than premature babies. However, pathologically, more premature babies suffered from HIE than term babies. HIE manifests clinically as symptoms of consciousness changes that can be excitatory like seizures or depressing like coma. Treatment of HIE focuses on monitoring, controlling seizures, maintaining circulation and glucose levels, with therapies like hypothermia and investigates like amplitude integrated EEG shown to improve outcomes. The prognosis depends on the severity of brain damage and treatment, with mild cases often having a full recovery but severe cases having a high risk of mortality or neurological sequele like cerebral palsy.
Acute kidney injury (AKI), formerly called acute renal failure, is a sudden deterioration of renal function that results in the buildup of waste products and fluid overload. It ranges from a minor increase in creatinine to complete kidney failure. Causes include decreased blood flow to the kidneys (prerenal), direct kidney damage (intrarenal), or urinary tract obstruction (postrenal). Symptoms include decreased urine output, retention of waste products, fluid overload, and electrolyte imbalances. Treatment focuses on fluid management, treating the underlying cause, and dialysis in severe cases. Chronic kidney disease (CKD) is the gradual loss of kidney function over time defined as kidney damage and/or decreased G
Approach to a child with HepatosplenomegalySunil Agrawal
This document discusses hepatosplenomegaly, or the enlargement of the liver and spleen. It begins with an introduction and overview of hepatomegaly and splenomegaly. It then covers the various causes of hepatosplenomegaly including infections, hematological disorders, vascular congestion, tumors and infiltrations, storage disorders, and miscellaneous causes. The document provides details on evaluating a patient's history, physical examination findings, investigations, and treatment strategies for hepatosplenomegaly in both children and neonates. It concludes with references for further information.
Neonatal sepsis is a clinical syndrome characterized by signs and symptoms of infection in the first month of life. It can involve sepsis, meningitis, pneumonia and other infections. The document discusses the definition, classification, risk factors, clinical features, investigations and management of neonatal sepsis. Key points include that sepsis is a leading cause of neonatal mortality, the importance of sepsis screening and blood cultures, and that initial empirical antibiotic therapy typically involves ampicillin and an aminoglycoside.
This presentation focuses on Acute Bacterial Meningitis.
Viral and fungal cause is mentioned but focus is on bacterial meningitis in Pediatrics Patient.
Feel free to correct if there is any error.
Refer to other reference books for clarity.
This document discusses malaria in children, including its classification, epidemiology, etiology, clinical features, complications, management, prognosis and prevention. It provides details on the life cycle and transmission of the plasmodium parasite. For diagnosis, it recommends looking for malarial parasites in blood smears or using rapid diagnostic tests. It describes the clinical features of malaria as fever, often alternating daily or every two days. Complications can include anemia, jaundice and cerebral malaria. Management involves antipyretics, hydration, nutrition and antimalarial drugs depending on the plasmodium species and local resistance patterns. Prevention methods are use of mosquito nets and chemoprophylaxis. The document also briefly discusses visceral
A preterm newborn developed respiratory distress soon after birth, with signs including grunting and cyanosis. Evaluation found respiratory distress syndrome (RDS). The baby was treated with nasal CPAP, surfactant, and mechanical ventilation. RDS is caused by surfactant deficiency in premature infants, resulting in alveolar collapse and impaired gas exchange. Management includes respiratory support, surfactant replacement therapy, and care to prevent complications.
This document discusses prematurity and its complications. It defines prematurity as infants born before 37 weeks gestation according to the WHO. Prematurity is classified based on gestational age as extremely, very, or moderate to late preterm. It can also be classified based on birth weight as low, very low, or extremely low. Risk factors include socioeconomic status, previous prematurity, and maternal health conditions. Causes include fetal, uterine, maternal, and iatrogenic factors. Clinical presentation includes weak reflexes and poor muscle tone. Complications involve respiratory, cardiovascular, gastrointestinal, metabolic, central nervous system, renal, and infectious issues. Long term complications may include developmental delays. Care after birth focuses on stabilization, monitoring,
This document discusses neonatal jaundice (hyperbilirubinemia) in infants. It covers the definition, causes, types (physiological vs pathological), investigations, management including phototherapy and exchange transfusion, and prevention of kernicterus. Key points include:
- Jaundice is caused by high bilirubin levels which cause yellowing of the skin and eyes. Bilirubin is produced from the breakdown of red blood cells.
- Physiological jaundice appears after 24-72 hours and is common, while pathological jaundice appears within 24 hours and requires treatment.
- Management involves phototherapy to reduce bilirubin levels or exchange transfusion for severe
Management of child with neonatal jaundiceNEHA MALIK
Newborn jaundice is a yellowing of a baby's skin and eyes. Newborn jaundice is very common and can occur when babies have a high level of bilirubin, a yellow pigment produced during normal breakdown of red blood cells.
follow me on my YouTube channel :- medic o mania
Neonatal jaundice (hyperbilirubinemia) by Rajiv MavachiRajiv Mavachi
Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
Primary Newborn Care: Management of important problemsSaide OER Africa
1. Jaundice is caused by high levels of bilirubin in the blood and can become dangerous at very high levels when bilirubin enters the brain.
2. Physiological jaundice is mild jaundice that is common in newborns, while abnormal jaundice requires treatment and may be caused by infections, blood incompatibilities, or other issues.
3. Phototherapy uses light to change bilirubin into a form that can be excreted from the liver, lowering bilirubin levels to prevent brain damage in infants with dangerous jaundice.
1. Jaundice is a yellowish discoloration of the skin and eyes caused by high bilirubin levels. It is often a sign of liver, gallbladder or pancreatic problems.
2. Bilirubin is produced from the breakdown of red blood cells and normally processed by the liver. Elevated bilirubin can be due to pre-hepatic issues affecting red blood cell breakdown, hepatic issues affecting the liver's ability to process bilirubin, or post-hepatic issues blocking bile ducts.
3. Evaluation of jaundice involves medical history, physical exam assessing skin and abdominal signs, and lab tests of liver function and imaging of the abdomen. Treatment
Physiological neonatal jaundice is caused by increased bilirubin production from the breakdown of fetal red blood cells combined with the immature liver's reduced ability to process bilirubin in newborns. The mechanisms involved include a higher rate of red blood cell destruction, insufficient albumin transport of bilirubin, and an immature hepatic system with low bilirubin conjugating enzyme activity. This causes bilirubin levels to rise after birth but then resolve on their own without treatment within 14 days.
Neonatal jaundice is the yellowish discoloration of skin due to high bilirubin levels. It can be physiological, appearing 2-3 days after birth and resolving in 10-12 days, or pathological, appearing within 24 hours. Physiological jaundice is caused by the normal breakdown of red blood cells in newborns. Pathological jaundice has underlying causes that interfere with bilirubin production, transport, conjugation or excretion. Mild cases are monitored while moderate-severe cases may require phototherapy or phototherapy with medication to process the bilirubin for excretion.
Hyperbilirubinemia is a condition where there is too much bilirubin in the blood, causing jaundice. Jaundice appears as a yellowing of the skin and eyes. The most common causes are physiologic jaundice in newborns and breast milk jaundice in breastfed babies. Hyperbilirubinemia is diagnosed by measuring bilirubin levels in the blood and treated with phototherapy or exchange transfusions for severe cases. Preventive measures focus on early detection and treatment to prevent high bilirubin levels.
Jaundice is a yellowish pigmentation of the skin and mucous membranes caused by high bilirubin levels in the blood (hyperbilirubinemia). Bilirubin is produced from the breakdown of heme in red blood cells and is normally processed by the liver and excreted in bile or urine. Jaundice can be physiologic in newborns or pathologic due to liver disease, hemolytic disease, or bile duct obstruction. The type of jaundice is determined by measuring conjugated and unconjugated bilirubin levels and depends on whether the cause is excessive bilirubin production, impaired liver function, or bile duct blockage.
This document discusses neonatal jaundice (hyperbilirubinemia). It defines jaundice as an excessive level of bilirubin in the blood characterized by yellowing of the skin. It distinguishes between physiological and pathological jaundice. The causes, pathophysiology, complications, diagnostic evaluation and management including phototherapy, exchange transfusion and drugs are described in detail over multiple pages.
Neonatal jaundice is caused by an accumulation of unconjugated bilirubin in the blood and tissues. Physiological jaundice appears between 2-4 days of life, peaks at 5-6 mg/dL by days 2-4, and resolves by days 5-7. Pathological jaundice appears within 24 hours, bilirubin increases more than 5 mg/dL per day, persists past 14 days, or direct bilirubin is elevated. Causes include hemolytic diseases, breastfeeding, infections, and genetic disorders affecting bilirubin metabolism. Timely diagnosis and treatment are important to prevent neurotoxicity and kernicterus.
The document summarizes heme catabolism and bilirubin metabolism. It discusses:
1) How bilirubin is formed from the breakdown of heme in reticuloendothelial cells, transported to the liver bound to albumin, and conjugated to a water-soluble form in hepatic cells for excretion.
2) The types of jaundice that can occur due to increased bilirubin levels, including hemolytic, hepatocellular, and obstructive jaundice.
3) Methods for diagnosing jaundice by measuring bilirubin levels in serum and urine using the Van Den Bergh reaction and assessing urine bilirubin and urobil
The document provides information about liver function tests and bilirubin metabolism. It discusses that liver function tests measure enzymes and proteins to evaluate how well the liver is performing its normal functions. Bilirubin is produced from the breakdown of heme in red blood cells and is metabolized and excreted by the liver. Elevations in bilirubin or certain enzymes in the blood can indicate liver disease or damage. Tests of bilirubin, enzymes, bile salts, and other substances in blood and urine are used to evaluate liver function and diagnose liver conditions.
This document provides an overview of conjugated hyperbilirubinemia in older infants and children. It begins with an introduction to jaundice and bilirubin metabolism. The main causes of conjugated hyperbilirubinemia discussed are extrahepatic biliary atresia, "idiopathic" neonatal hepatitis, and Alagille syndrome. Extrahepatic biliary atresia is the most common cause and involves a progressive inflammatory process affecting the biliary tree. "Idiopathic" neonatal hepatitis refers to cases where no clear cause is identified. Alagille syndrome is a genetic disorder characterized by bile duct paucity and other cardiac, facial and skeletal abnormalities. The document provides details on
This document summarizes bilirubin metabolism and hyperbilirubinemia. It describes how bilirubin is produced from the breakdown of hemoglobin, and the normal pathway of conjugation and excretion. For newborns, the higher rate of bilirubin production and immature liver enzymes can lead to physiologic jaundice. Unconjugated hyperbilirubinemia can result from hemolysis or liver dysfunction, while conjugated hyperbilirubinemia indicates liver or biliary issues. The potential complication of severe hyperbilirubinemia is kernicterus or bilirubin-induced neurological damage.
Management of hiperbilirubic infant finalkinjalisha
Hyperbilirubinemia or jaundice in newborns, known as neonatal jaundice, is common. It occurs when bilirubin levels are elevated, causing a yellowing of the skin and eyes. The document discusses what neonatal jaundice is, how bilirubin is formed and metabolized, common causes of jaundice including physiological and pathological factors, clinical manifestations, diagnostic evaluation, classification, risk factors and various treatment approaches including phototherapy.
Breast milk jaundice.
The key features that point to breast milk jaundice in this case are:
- Jaundice onset after the first week of life
- Progressive deepening of jaundice over 1 week
- Exclusively breastfed
- Pale/gray stool color indicating reduced bilirubin conjugation
Breast milk jaundice results from high levels of beta-glucuronidase in breast milk interfering with bilirubin conjugation in the infant's liver and gut. It typically presents after the first week of life and can persist for several weeks if breastfeeding continues.
The document summarizes information about liver function tests and bilirubin metabolism. It discusses:
- Liver function tests measure enzyme and protein levels to evaluate liver health and function. They can screen for disease, determine disease patterns, and assess severity and treatment response.
- Bilirubin is produced from the breakdown of heme in red blood cells. The liver conjugates bilirubin so it can be excreted in bile or urine. Elevated bilirubin levels can indicate liver damage or blockages.
- Tests are classified based on the liver's excretory, detoxification, synthetic and metabolic functions. Enzymes like AST, ALT and GGT are also measured
Asp openly licensed stories for early reading in africa mar 2015 slideshareSaide OER Africa
A recent presentation made by Tessa Welch, the African Storybook Project leader, to University of Pretoria Education students on the project and on openly licensed stories for early reading in Africa.
Quality Considerations in eLearning in South Africa. Presentation at the eLearning Summit, Indaba Hotel, 16 October 2014. Looks the the quality review process and quality criteria.
African Storybook: The First 18 Months of the ProjectSaide OER Africa
Presentation by African Storybook Initiative Leader, Tessa Welch, on the first 18 months of the initiative. Presented on 26 June at the African Storybook Summit at the University of British Columbia.
Digital Storytelling for Multilingual Literacy Development: Implications for ...Saide OER Africa
Digital Storytelling for Multilingual Literacy Development: Implications for Teachers - Presentation by Tessa Welch at the South African Basic Education Conference 31 March - 1 April 2014. Presentation explains Saide's African Storybook Initiative. Overview: Requirements for effective literacy development of young children in African countries; obstacles to achieving this goal; multi-pronged approach to overcoming obstacles; examples of digital storytelling in a school community; implications for teachers.
This document provides an overview of technology trends and outlook for African higher education. It discusses key drivers and constraints to integrating technology, including motivators like access to resources and constraints like low digital fluency of faculty. Current trends include growing social media usage, blended learning, and data-driven assessment. The document outlines different modes of educational provision from fully offline to fully online. It provides an outlook on emerging technologies like flipped classrooms, learning analytics, and 3D printing and their potential impact on higher education in both the short and long term. The talk concludes by emphasizing that technology should support, not replace, good teaching practices.
eLearning or eKnowledge - What are we offering students?Saide OER Africa
eLearning or eKnowledge - What are we offering students? A look at the convergence of elearning and eknowledge, looking at the purpose of the design - informational or instructional? Presented at the Unisa Cambridge Open and Distance eLearning Conference, Stellenbosch.
Presentation given at the Online and eLearining Conference organised by Knowledge Resources at the Forum, Bryanston, Johannesburg 28-29 August 2013. Created by Greig Krull, Sheila Drew and Brenda Mallinson.
Understand school leadership and governance in the South African context (PDF)Saide OER Africa
This module gives an overview of what management and leadership is about in a school setting. As an aspiring principal it begins a process of developing understanding about the challenges that face principals on a daily basis and allows you to also explore your own realities and decide on new and better action. In addition, you will look at some of the international trends in management and leadership and will compare what is happening in the South Africa scene to others.
Toolkit: Unit 8 - Developing a school-based care and support plan.Saide OER Africa
The document provides guidance to school management teams on developing a school-based care and support plan. It includes tools to help schools analyze the needs of vulnerable learners, create a vision statement, conduct a SWOT analysis, and identify strategic goals. The tools would help schools understand the challenges they face in supporting vulnerable students, develop a plan to address these challenges, and establish goals and objectives in key areas like nutrition, aftercare, counseling, and HIV/AIDS education.
Toolkit: Unit 7 - Counselling support for vulnerable learners.Saide OER Africa
The purpose of this toolkit is to conduct a situational analysis or assessment that will help you to understand the size of the challenge and the current capacity of your school to set up a counselling service. To assist you to decide on the most suitable options for implementing counselling support in your school context.
The purpose of this toolkit is to use a brainstorming technique to come up with creative ideas respond to the challenge of providing aftercare support for vulnerable learners. To use the ideas from the brainstorming session to inform the development of a draft set of ideas for an aftercare strategy.
There are different ways of combating discrimination and creating a safe and nonthreatening environment at school. An important contribution can be made by implementing an Anti-Bullying Policy
The guidelines and the five priority areas identified by Department of Education offer a framework that supports the development of a school HIV and AIDS policy. The guidelines and priorities can also be used to review your school's existing HIV and AIDS policy and determine how adequate it is and what changes may be necessary
Toolkit: Unit 1 - How responsive are schools to the socio-economic challenges...Saide OER Africa
The purpose of this toolkit is to understand what threatens the quality of education in your school so that you can take informed action to remedy the situation.
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Here are a few key points about Joseph based on the description:
- He struggles to focus, follow instructions, and complete work. This suggests difficulties with attention, executive functioning, and/or self-regulation.
- He is easily distracted and fidgety. This could indicate an attention issue like ADHD.
- He has quick temper outbursts. This points to potential difficulties with emotional regulation.
- The water spill incident triggered an extreme reaction, rather than a calm response like Martha's. This reinforces the idea of challenges with emotional control.
Overall, Joseph seems to exhibit signs of difficulties with attention, self-control, and emotional regulation - all of which could interfere with his ability to function
Reading: Understanding Intrapersonal Characteristics (pdf)Saide OER Africa
The impact of intrapersonal characteristics on school performance and learner development - A reading to accompany Unit Six of the module: Teaching and Learning Mathematics in Diverse Classrooms. This reading is useful because it summaraizes the various theoretical perspectives for understanding inclusive education, and because it uses case studies of typical learners to illustrate how teaching and learning activities need to be adapted to ensure that all children, no matter what their background or intrapersonal characteristics do learn mathematics.
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A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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Executive Directors Chat Leveraging AI for Diversity, Equity, and InclusionTechSoup
Let’s explore the intersection of technology and equity in the final session of our DEI series. Discover how AI tools, like ChatGPT, can be used to support and enhance your nonprofit's DEI initiatives. Participants will gain insights into practical AI applications and get tips for leveraging technology to advance their DEI goals.
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
1. 9
Jaundice,
anaemia and
polycythaemia
JAUNDICE
Objectives
9-1 What is jaundice?
When you have completed this unit you
should be able to: Jaundice is the yellow colour of the skin and
sclerae caused by deposits of bilirubin. In
• Define jaundice and
newborn infants the sclerae (white of the eye)
hyperbilirubinaemia. are difficult to see and, therefore, the skin
• Describe the excretion of bilirubin. colour is used to detect jaundice. Jaundice is a
• List the causes of jaundice. clinical sign and not a laboratory measurement.
• List the dangers of hyperbilirubinaemia.
• Understand haemolytic disease of the Neonatal jaundice is a yellow colour of the skin
newborn. caused by bilirubin
• Treat jaundice.
• List the common causes and treatment
of anaemia. 9-2 What is bilirubin?
• List the common causes and treatment Red blood cells contain a red pigment called
of polycythaemia. haemoglobin which carries oxygen. Red
cells in the fetus and newborn infant live
for 3 months only. Therefore, the body is
continually forming new red cells in the bone
marrow to replace the old red cells which are
broken down in the liver and spleen.
When red cells die, their haemoglobin is
changed into a yellow pigment called bilirubin.
This unconjugated bilirubin is carried by
2. 164 NEWBORN CARE
albumin in the blood stream to the liver to separate the serum from the red cells. The
where it is first conjugated (joined to another total serum bilirubin (TSB) is then measured
substance) and then excreted in the bile. If with a bilirubinometer and expressed in
the concentration of bilirubin in the serum μmol/l. The TSB includes both unconjugated
(blood) rises, it becomes visible in the skin and conjugated bilirubin. However, in the
causing jaundice. Newborn infants normally newborn infant the TSB usually consists
have a high haemoglobin concentration and, mainly of unconjugated bilirubin.
therefore, produce a lot of bilirubin.
The total serum bilirubin (TSB) cannot be
Normal newborn infants produce a lot of bilirubin estimated accurately by clinically assessing the
degree of jaundice in the skin
9-3 What is hyperbilirubinaemia? NOTE The degree of jaundice can be measured
Hyperbilirubinaemia is defined as concen- with a transcutaneous bilirubinometer. However,
tration (level) of total serum bilirubin (TSB) the monitors are expensive, easily damaged and
of limited accuracy once phototherapy has been
that is higher than the normal range. Normally
started. They are useful in screening infants for
the bilirubin concentration in the serum
phototherapy.
is low at birth, less than 35 μmol/l. It then
climbs steadily for the first few days before
returning again to an adult level of less than 9-5 How is bilirubin excreted in the adult?
35 μmol/l by 2 weeks. The total serum bilirubin Unconjugated bilirubin, formed by the
concentration in term infants usually does not breakdown of red cells, is carried by albumin in
rise above 200 μmol/l (12 mg/dl). the blood stream to the liver. In the liver cells
The upper limit of the total serum bilirubin enzymes combine the unconjugated bilirubin
concentration (TSB) in most healthy term with glucuronic acid to form conjugated
infants is approximately: bilirubin. This chemical process, called
conjugation, makes the bilirubin water soluble.
Days after birth 0 0.5 1 Only when the bilirubin is water soluble can
TSB (μmol/l) 35 75 125 the liver cells excrete it into the small bile
ducts. From here the conjugated bilirubin is
Days after birth 2 3 4 5 carried in the bile to the intestine where it is
further converted by bacteria into the brown
TSB (μmol/l) 150 175 200 200
pigment, stercobilin. In the adult, bilirubin is
NOTE The upper limit of the normal total serum
not reabsorbed from the intestine. Therefore
bilirubin concentration is very controversial. In the final breakdown products of bilirubin are
healthy, term, breastfed infants the upper limit passed in the stool.
may be as high as 275 μmol/l.
Conjugation of bilirubin in the liver is essential
9-4 How is bilirubin measured?
before it can be excreted into the bile
It is both difficult and inaccurate to assess
the concentration of bilirubin in the serum
by clinical examination of the degree of 9-6 How is bilirubin excreted in the fetus?
jaundice, especially in an infant with a dark The fetus is unable to excrete conjugated
skin. Therefore, it is important to measure bilirubin via the stool as it usually does not
the bilirubin concentration of the serum if an pass meconium and also lacks bacteria in the
infant is jaundiced. Usually a sample of blood is intestines to convert bilirubin into stercobilin.
collected into a capillary tube and spun down Instead, fetal bilirubin, is excreted by the
3. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 165
placenta into the mother’s blood. However,
Jaundice during the first 24 hours is always
the placenta can only remove fat soluble,
abnormal
unconjugated bilirubin and not water soluble,
conjugated bilirubin. To ensure that most
of the fetal bilirubin remains unconjugated, NOTE The reabsorption of bilirubin from the
intestine back into the blood stream of newborn
the enzyme system that controls bilirubin
infants (enterohepatic circulation of bilirubin)
conjugation in the liver functions very slowly. is due to the enzyme β glucuronidase in the
The small amount of conjugated bilirubin bowel wall. This enzyme is also present in
that is excreted into the bile is carried to the breast milk resulting in a higher TSB in breastfed
fetal intestine. Here a special fetal enzyme infants. As a result, some normal breastfed
deconjugates the bilirubin, which is then infants remain jaundiced for more than two
reabsorbed back into the fetal blood stream as weeks (breast milk jaundice).
unconjugated bilirubin. In this way the fetus
ensures that all the bilirubin can be excreted 9-8 What are the causes of jaundice?
by the placenta.
The main causes of jaundice in the newborn
infant are:
Bilirubin in the fetus is excreted by the placenta 1. Increased production of bilirubin
rather than the liver 2. Slow bilirubin conjugation in the liver
3. Decreased excretion of bile
9-7 How is bilirubin excreted in the
9-9 What are the causes of an increased
newborn infant?
production of bilirubin?
During the first week of life the enzyme system
There are many causes of an increased
that conjugates bilirubin with glucuronic acid
bilirubin production:
in the liver functions slowly, as in the fetus.
Therefore, unconjugated bilirubin accumulates 1. The normal newborn infants produces a
in the serum as the placenta is no longer lot of bilirubin due to a high haemoglobin
present to remove it. As a result, newborn concentration.
infants commonly become jaundiced due to 2. Cephalhaematoma or bruising.
an increased concentration of unconjugated Haemoglobin which has escaped out of
bilirubin in the serum. After a few days the damaged blood vessels is rapidly broken
rate of liver conjugation increases and the down into bilirubin which is absorbed
bilirubin concentration in the serum slowly back into the blood stream.
returns to the normal adult range of less than 3. Polycythaemia. Infants with a very high
35 μmol/l. Jaundice at birth or in the first packed cell volume or haemoglobin
24 hours is unusual, however, as the bilirubin concentration have excess haemoglobin
is adequately excreted by the placenta up until and, therefore, produce a lot more bilirubin
the time of delivery. than normal.
4. Infection. General infections such as
Some of the bilirubin that is conjugated and
septicaemia and syphilis cause haemolysis
excreted by the liver in the first week of life
(breakdown of red cells). The released
is broken down by the fetal enzyme in the
haemoglobin is converted into bilirubin.
intestine which continues to function for a few
5. Haemolytic disease of the newborn.
weeks after birth. This unconjugated bilirubin
Excess haemolysis causes an increased level
is reabsorbed by the intestine, adding to the
of unconjugated bilirubin.
increase of the TSB.
NOTE Excessive haemolysis may rarely be due
to deficiency of a red cell enzyme (e.g. glucose
6 phosphate dehydrogenase deficiency), an
4. 166 NEWBORN CARE
abnormal red cell membrane (e.g. spherocytosis) birth as they reabsorb some unconjugated
or an abnormal haemoglobin (e.g. alpha bilirubin from the intestine back into the
thalassaemia). blood stream. As a result, jaundice with a
raised unconjugated bilirubin is common
9-10 What are the causes of slow bilirubin in breastfed infants.
conjugation? 2. Hepatitis due to septicaemia, viral
1. Normal, healthy, term infants have a slow infection or syphilis. Swelling of the liver
bilirubin conjugation for the first week cells obstructs the flow of bile in the small
after delivery. The liver of the newborn bile ducts.
infant during the first few days of life, 3. Biliary atresia is destruction of the bile
therefore, functions like that of the fetus. ducts caused by a viral infection during the
2. About 10% of clinically healthy, term first weeks of life.
infants have a TSB that increases above the Diseases of the liver (hepatitis and biliary
normal range. They have a greater than atresia) prevent the excretion of conjugated
usual delay in the maturation of their liver bilirubin into the bile. Conjugated bilirubin is,
enzymes responsible for conjugation. therefore, reabsorbed into the blood stream,
3. Preterm infants also commonly have a resulting in jaundice. This is called obstructive
TSB that rises above the normal range jaundice, and can be diagnosed by finding a
due to immaturity of their liver enzymes. high concentration of conjugated bilirubin
This is known as jaundice of immaturity. in the serum. If bilirubin cannot be excreted
Jaundice is commoner in preterm than in in the bile, the stools become pale. Some of
term infants. the excess conjugated bilirubin is excreted by
4. Congenital hypothyroidism due to the the kidneys, giving dark urine. Jaundice due
absence of a thyroid gland in the infant to decreased excretion of bilirubin is far less
may cause prolonged jaundice due to slow common in newborn infants than jaundice
maturation of the liver enzymes. Although due to the excessive production or decreased
rare, it is important as these children conjugation of bilirubin.
become severely mentally retarded if not
diagnosed and treated soon after birth.
They need lifelong thyroxine treatment. Pale stools and dark urine suggest that the
jaundice is due to liver disease
In all these conditions, with an increased
production or slow conjugation of bilirubin,
the serum bilirubin is unconjugated. 9-12 What is physiological jaundice?
All healthy newborn infants have a total serum
Prolonged jaundice may be due to hypothyroidism bilirubin concentration (TSB) higher than in
adults. This is due to the normal increase in
NOTE In some countries all newborn infants are production, slow conjugation and decreased
screened for hypothyroidism. Thyroid stimulating excretion of bilirubin. As a result, 50% of
hormone (TSH) and thyroxine (T4) are measured normal, term infants have mild jaundice
in infant blood collected at birth or within a during the first 2 weeks of life. However, they
few days after delivery. A high TSH and low T4 are clinically well, their jaundice disappears
suggests hypothyroidism.
within 14 days and their TSB does not rise
above 200 μmol/l (12 mg/dl). This is known
9-11 What causes a decreased excretion of as physiological jaundice. Mild jaundice is,
bilirubin? therefore, very common in normal infants.
1. Healthy breastfed infants have a decreased
excretion of bilirubin for a few weeks after
5. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 167
Therefore, a person with both A and D
Mild jaundice in healthy infants is very common
antigens will have the A positive blood group
in the first two weeks of life
while another with neither A, B nor D antigens
will be blood group O negative.
NOTE Some studies suggest that in physiological
jaundice the TSB may rise as high as 275 μmol/l.
9-15 What is ABO haemolytic disease?
ABO haemolytic disease occurs when the
HAEMOLYTIC DISEASE mother is blood group O and her fetus is blood
group A or B, the fetus having inherited these
blood groups from the father. For reasons
9-13 What is haemolytic disease of the unknown, some group O mothers start
newborn? producing anti-A or anti-B antibodies which
Haemolytic disease of the newborn is the cross the placenta and cause fetal haemolysis
condition where antibodies (immunoglobulins) by attacking the fetal red cells. The haemolysis
from the mother cross the placenta into the is not severe enough to damage the fetus but
fetal blood stream. Here these antibodies may cause severe jaundice in the newborn
destroy the fetal red cells (haemolysis) causing infant. ABO haemolytic disease may occur in a
anaemia and an increased production of first pregnancy or any later pregnancy.
bilirubin in the fetus and newborn infant. The maternal antibodies, which stick to the
The 2 most important causes of haemolytic fetal red cells, give a positive Coomb’s test in the
disease of the newborn are: newborn infant, while the haemolysis results
in a low packed cell volume and haemoglobin,
1. ABO haemolytic disease and a raised TSB. An infant with ABO
2. Rhesus haemolytic disease haemolytic disease usually appears normal
There are also other uncommon forms of at delivery, as the placenta has been able to
haemolytic disease in newborn infants. remove the excess bilirubin produced during
pregnancy. However, the infant becomes
jaundiced within the first 24 hours after birth.
9-14 What are blood groups?
The TSB may increase rapidly and reach
Red cells have proteins on their surface called dangerous levels. Due to the haemolysis, the
antigens, which determine a person’s blood infant becomes anaemic. Unfortunately ABO
group. The red cell antigens of a fetus are inheri- haemolytic disease is not preventable nor can
ted from both parents and, therefore, may differ it be diagnosed accurately before delivery.
from that of the mother. The most important ABO haemolytic disease is the commonest
red cell antigens are the ABO antigens and the cause of severe jaundice in term infants.
D (Rhesus) antigen. If the A antigen is present
on a person’s red cells the blood group will
be A. Similarly, the presence of the B antigen
ABO haemolytic disease is the commonest cause
makes the blood group B. If both antigens are of severe jaundice in term infants
present the blood group will be AB while if
both antigens are absent the blood group will NOTE In ABO haemolytic disease the mother
be O. Most people are blood group O. produces IgG antibodies to A or B. These small
antibodies can cross the placenta and, therefore,
The D antigen is inherited separately from the differ from the large IgM antibodies to A and B
ABO antigens. The presence of the D antigen which are present in the serum of all group O
on the red cells makes a person Rhesus positive. adults. It is not understood why some women
If the D antigen is missing, then the person is produce IGg antibodies to A and B antigens.
Rhesus negative.
6. 168 NEWBORN CARE
9-16 How do you diagnose ABO haemolytic as it only occurs if fetal blood crosses the
disease at birth? placenta (a fetomaternal bleed) to reach the
mother’s blood and, thereby, sensitises her
1. The mother is blood group O.
into producing anti-D antibodies. Rhesus
2. The father is blood group A, B or AB.
haemolytic disease becomes progressively
3. The infant is blood group A or B.
worse with each further pregnancy. Unlike
4. The Coomb’s test is positive in the infant.
ABO haemolytic disease, with Rhesus
5. The TSB is often high (above 35 μmol/l)
haemolytic disease the degree of fetal
while the haemoglobin and packed cell
haemolysis is severe and the fetus may go into
volume is often low (below 45%) in the
heart failure with resulting generalised oedema
cord blood.
(called hydrops) due to anaemia and die.
6. The infant commonly develops jaundice
Fortunately Rhesus haemolytic disease is not
within 24 hours of delivery. The jaundice
common, because most people are Rh positive.
usually increases rapidly and the TSB may
Rhesus haemolytic disease can be prevented.
reach dangerous levels during the first week.
7. The TSB at 6 hours after delivery is often NOTE The Rhesus blood group is named after the
above 80 μmol/l. Rhesus monkey used in early experiments with
red cell antigens. Rhesus haemolytic disease can
also be caused by other Rhesus antigens (C, c, E
Jaundice on day 1 suggests haemolytic disease and e). These forms are less severe than Rhesus
haemolytic disease due to the D antigen (Rh D
haemolytic disease).
9-17 What is Rhesus haemolytic disease? Fetal red cells may cross the placenta into the
Rhesus haemolytic disease is haemolytic mother’s blood:
disease of the newborn caused by maternal 1. At delivery (the most common)
antibodies to the D antigen. With Rhesus 2. During a miscarriage
haemolytic disease, the mother is always 3. With abruptio placentae
Rhesus negative (Rh negative or Rh –ve) while 4. During amniocentesis
the fetus and infant (and father) are always 5. During external cephalic version
Rhesus positive (Rh positive or Rh +ve).
Normally the fetal red blood cells do not enter The fetus can die of Rhesus haemolytic disease
the maternal circulation during pregnancy
or delivery. However, if the fetal capillaries in
the placenta are damaged, fetal red blood cells 9-18 How can you prevent Rhesus
may cross into the maternal blood. If the fetal haemolytic disease?
red cells have the D antigen (Rh positive) but
the mother’s do not (Rh negative), then the The Rh positive fetal red cells that cross the
fetal cells may be recognised by the mother’s placenta can be destroyed, before they sensitise
immune system as foreign. As a result the Rh- the mother, by giving her 100 μg (4 ml) anti-D
negative mother will respond by producing immunoglobulin by intramuscular injection
antibodies (anti-D) against these foreign red within 72 hours. This is usually given after
cells. This process is known as sensitisation. delivery of an Rh-negative mother. However,
Rarely an Rh-negative woman may also be anti-D immunoglobulin must also be given
sensitised against the D antigen if she receives after any of the above complications of
an incompatible blood transfusion with Rh pregnancy. Unfortunately it is useless giving
positive red cells. the mother anti-D immunoglobulin if she has
already been sensitised and has developed her
Rhesus haemolytic disease is more severe own anti-D antibodies.
than ABO haemolytic disease. Rhesus
haemolytic disease is rare in first pregnancies
7. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 169
bilirubin may then enter the brain of
Give all Rhesus-negative mothers anti-D
the newborn infant and cause bilirubin
immunoglobulin after delivery
encephalopathy (kernicterus). Conjugated
bilirubin is not toxic to the brain. In clinical
practice the TSB is used to assess whether the
9-19 How can you diagnose Rhesus
bilirubin is reaching dangerous concentrations
haemolytic disease during pregnancy?
as the TSB in newborn infants usually consists
1. Mother’s blood group is Rhesus negative. almost entirely of unconjugated bilirubin.
2. Father’s blood group is Rhesus positive.
The risk of bilirubin encephalopathy depends
3. Mother has anti-D antibodies in her blood.
on:
4. Mother may have had a previous infant
with jaundice or a past obstetric history 1. The total serum bilirubin concentration.
which suggests a fetomaternal bleed. The higher the TSB, the greater is the
Usually the mother would not have chance that unconjugated bilirubin will
received anti-D immunoglobulin after her cross the blood brain barrier into the
previous deliveries. brain cells.
2. The gestational age. The more preterm
The blood group of all pregnant women
the infant the higher the risk due to an
should be determined at the start of antenatal
immature blood brain barrier.
care. If you suspect that the pregnancy is
3. The postnatal age. A high TSB in the first
complicated by Rhesus haemolytic disease (i.e.
few days has a greater chance of increasing
a Rh-negative patient with anti-D antibodies),
to dangerous levels than the same TSB at a
the mother must be referred urgently to a
week of age.
hospital where specialist care is available.
4. Factors that may make the blood brain
barrier more permeable to bilirubin, such
All women must have their blood groups as hypoxia, hypothermia, hypoglycaemia
identified during pregnancy and infection.
NOTE The blood brain barrier is a complex mech-
Rhesus haemolytic disease should be anism that prevents toxic substances like bilirubin
considered if the infant is jaundiced, pale and crossing from the blood into the brain cells.
oedematous in the first 24 hours of life. Severe In well, term infants the TSB becomes
Rhesus haemolytic disease affecting the fetus dangerous above 350 μmol/l (20 mg/dl)
can be diagnosed during pregnancy if antenatal while in preterm infants the TSB becomes
ultrasound examination shows signs of fetal dangerous above 250 μmol/l (15 mg/dl). The
oedema and heart failure (hydrops fetalis). dangerous level is lower if factors that make
the blood brain barrier more permeable to
Rhesus haemolytic disease should be diagnosed bilirubin are also present.
during pregnancy
A high serum concentration of unconjugated
NOTE Antenatal Doppler ultrasound can be used bilirubin can damage the brain
to identify anaemic fetuses while new technology
can determine the fetal blood group on a sample
of maternal blood.
9-21 How do you recognise bilirubin
encephalopathy?
9-20 Is jaundice dangerous?
1. The infant is very jaundiced.
Jaundice can become dangerous when the 2. The TSB is very high.
concentration of unconjugated bilirubin in
the blood becomes very high. Unconjugated
8. 170 NEWBORN CARE
3. At first the infant is lethargic, hypotonic, from where it can easily be excreted without
has a weak cry, poor Moro reflex and feeds first having to be conjugated. Phototherapy
poorly with vomiting due to depressed is, therefore, able to rapidly lower the TSB.
brain function. Bright light is able to change the shape but
4. Later the infant becomes irritable with a not the chemical composition of the bilirubin
high-pitched cry, jitteriness, opisthotonus molecule. Ultraviolet light, which causes
and convulsions due to brain irritation. sunburn and severe tissue damage, could kill
an infant and is not used for phototherapy.
Many infants with bilirubin encephalopathy
die while the survivors are usually deaf and NOTE With phototherapy, unconjugated bilirubin
mentally retarded with hypotonic cerebral is converted by the process of photoisomerisation
palsy. Therefore, every effort must be made to into photobilirubin and lumirubin which are water
soluble and, therefore, easily excreted in the stool
prevent bilirubin encephalopathy.
and urine. Phototherapy does not conjugate
bilirubin. Blue light (at a wavelength of ) 455 nm
9-22 How can you prevent bilirubin is the most effective.
encephalopathy?
By not allowing the TSB to reach dangerous 9-24 What is used to give phototherapy?
levels. A number of methods can be used to Phototherapy is usually given with a
reduce the TSB: phototherapy unit which consists of a row
1. Give early milk feeds to reduce the amount of fluorescent tubes. Daylight tubes (SABS
of bilirubin that is reabsorbed from the No. 5) or white tubes (SABS No. 2) are used.
intestine. They should be changed after 1000 hours
2. Prevent preterm delivery. use as, despite still appearing bright, their
3. Give anti-D immunoglobulin to all effectiveness decreases with time and they
Rhesus-negative mothers after delivery, produce ultraviolet light which is dangerous.
a miscarriage, amniocentesis, abruptio A perspex (clear plastic) sheet must be placed
placentae or external cephalic version. below the tubes to reduce heat. A perspex
4. Give phototherapy when the TSB sheet also protects the infant if a fluorescent
approaches dangerous levels. tube breaks or comes loose. Sometimes a
5. Do an exchange transfusion when special white halogen spot light or blue LED
phototherapy cannot keep the TSB below (light emitting diode) spotlight is also used to
dangerous levels or when dangerous levels provide phototherapy.
have already been reached. Although exposure to sunlight also lowers the
TSB, an infant placed in the sun may rapidly
Early milk feeds help to lower the total serum become hyperthermic. Therefore, this form
bilirubin concentration of phototherapy must be used with great
caution, if at all.
NOTE The amount of light given out by the
phototherapy unit can be measured with a
PHOTOTHERAPY photometer. Only light in the blue part of the
spectrum is measured and the energy output
is given in μWatts/cm2/nm. An output above
9-23 What is phototherapy? 7μWatts is needed for effective phototherapy.
A phototherapy blanket can add to the amount
Phototherapy uses white or blue light (i.e. of phototherapy given by phototherapy lights.
visible light) to change unconjugated bilirubin However, it can only provide a limited amount
in the skin into a water-soluble form of of phototherapy if used alone. An advantage of
bilirubin. The water-soluble bilirubin is then LED spot lights is that they emit no ultraviolet
carried by albumin in the blood to the liver, light or heat.
9. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 171
TSB μmol/1
350
300
250
200
150
100
50
0
0 1 2 3 4 5 6 7
Age in days
Figure 9-1: Simple phototherapy guide for term infants showing the phototherapy line.
9-25 When should you give phototherapy? encephalopathy. Therefore, prophylactic
phototherapy is started immediately after
Phototherapy can be used either therapeutically
birth if haemolytic disease of the newborn
or prophylactically.
is suspected or diagnosed. Prophylactic
Therapeutic phototherapy should be given phototherapy in preterm infants is usually
whenever the TSB is above the normal range started when the TSB reaches 125 μmol/l in
and approaches dangerous levels. In practice infants weighing less than 1250 g, at 150 μmol/l
a simple chart is used to decide when to give in infants less than 1500 g, and at 200 μmol/l in
therapeutic phototherapy. If the TSB for the infants weighing less than 2000 g.
infant’s age reaches the phototherapy line,
treatment should be started. Phototherapy 9-26 How do you give phototherapy?
is usually started earlier in preterm or sick
infants. Phototherapy should not be given to 1. Switch on the phototherapy unit and make
healthy, term infants who are jaundiced with a sure the tubes are all working. Check
TSB below the phototherapy line. the age of the tubes and ensure that the
perspex sheet is in position.
All infants born to women who are blood 2. Place the infant naked in an incubator or
group O should have their TSB measured at 6 bassinet so that the mattress is about 40 cm
hours after birth. If the TSB is above 80 μg/dl from the phototherapy tubes. The infant
phototherapy should be started. must not wear a nappy. Instead, a nappy
With phototherapy it is possible to avoid can be placed under the infant.
almost all exchange transfusions. 3. Cover the infant’s eyes with pads as the
bright light worries the infant and may
Prophylactic phototherapy is given when the possibly damage the retina. Remove the
TSB is still below the phototherapy line but eye pads during feeding so that the eyes
either the TSB is expected to increase rapidly can be checked for infection and to allow
or the infant is at an increased risk of bilirubin the infant and mother to see each other.
10. 172 NEWBORN CARE
4. Turning the infant over every hour does and this may interfere with bonding.
not make the phototherapy more effective. Conjunctivitis may also be hidden by the
5. Feed the infant milk, at least every 3 to pads. Therefore, it is advisable to remove
4 hours. Breastfeed if possible. Add an extra the eye pads every time the infant is fed.
25 ml/kg/day if the infant is demand fed Replace the pads after the feed.
with formula. The lights may be switched off 4. Visible jaundice rapidly disappears under
during feeds or the infant may be removed phototherapy even if the TSB remains
from the phototherapy unit when fed. high or continues to increase. The TSB
6. Monitor the infant’s temperature hourly, must be monitored in all infants receiving
weigh twice a day and measure the TSB phototherapy.
daily or more frequently if it approaches 5. Other changes in skin colour may occur.
dangerous levels. After a few days the infant may become
7. Allow the mother unrestricted visiting. tanned. Erythema (a pink rash) may
If possible, the infant should be given result from excessive heat if a perspex
phototherapy next to the mother in the sheet is not placed below the tubes.
postnatal ward. Most skin rashes are aggravated by
phototherapy, and phototherapy given
9-27 For how long should you give in error to an infant with conjugated
phototherapy? hyperbilirubinaemia gives a grey/green
colour to the skin known as bronzing.
Continue phototherapy until the TSB has been 6. Phototherapy separates the infant from
under the phototherapy line for 24 hours. the mother and, therefore, should not be
Sometimes the TSB rises above the line again given unless there is a good reason. The
after the phototherapy has been stopped and separation caused by phototherapy results
treatment has to be restarted. However, once in maternal anxiety and also may prevent
the TSB drops it usually stays down. Most the establishment of breastfeeding.
phototherapy can be stopped after 3 days.
9-28 What are the dangers of The total serum bilirubin should be measured in
phototherapy? all infants receiving phototherapy
1. The infant may become too hot or too cold.
It is essential to monitor skin temperature 9-29 Can phenobarbitone be used to treat
very carefully during phototherapy. jaundice?
2. The infant may pass loose green stools,
due to the large amount of bilirubin There is little evidence that giving oral or
excreted into the gut. The infant may also intramuscular phenobarbitone adds to the
sweat more than usual. This may lead to effectiveness of phototherapy. It may also cause
excessive weight loss due to dehydration. lethargy and poor feeding. Phenobarbitone is,
When under phototherapy, breastfed therefore, not recommended to treat neonatal
infants should be allowed to feed at least jaundice. It should not be used instead of
every 4 hours while bottle-fed infants phototherapy.
should receive an extra 25 ml/kg/day as NOTE Phenobarbitone 5 mg/kg intravenously may
milk feeds. There is no need to give extra help lower the TSB in infants with severe jaundice.
clear feeds. All infants under phototherapy Clearing the meconium from the colon with a
should have their weight monitored. glycerine suppository may also help. In infants with
3. The infant’s eyes should be covered with Rh or ABO haemolytic jaundice, immunoglobulin
intravenously stops the haemolysis.
pads to prevent excessive exposure to
bright light. The pads prevent the mother
and infant seeing each other, however,
11. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 173
matching. Give phototherapy in the meantime.
Routine use of phenobarbitone to reduce
Remember that an exchange transfusion has
jaundice is not advised
its dangers and side-effects.
NOTE In an exchange transfusion, twice the
9-30 When is an exchange transfusion infant’s blood volume is exchanged with fresh
needed? compatible group O negative donor blood
Except for infants with severe Rhesus (160 ml/kg). Usually the exchange is done via
a catheter placed in the umbilical vein and
haemolytic disease, an exchange transfusion
10–20 ml blood is exchanged at a time. Care
is rarely needed today if phototherapy is should be taken to keep the infant warm and to
used correctly when indicated. However, an monitor vital signs during the procedure.
exchange transfusion may still be needed if
there is a delay in starting phototherapy and
the progressive increase in TSB cannot be ANAEMIA
controlled.
The indications for an exchange transfusion are:
9-31 What is anaemia?
1. A TSB above 400 μmol/l (20 mg/dl) in well
term infants despite phototherapy. To determine whether an infant has anaemia,
2. A TSB above 250 to 350 μmol/l (15 mg/dl) either of the following can be measured:
in well preterm infants depending on the 1. Packed cell volume (PCV), which is
weight of the infant. The smaller the infant expressed as a percentage.
the lower the TSB at which an exchange 2. Haemoglobin concentration (Hb), which is
transfusion is indicated. expressed in g/dl.
3. A lower TSB if the infant is or has been
hypoxic, hypothermic, hypoglycaemic or Anaemia is defined as a PCV or Hb that falls
infected. below the normal range for the postnatal age
4. A rapidly rising TSB and falling packed cell of the infant.
volume on day 1 in an infant with Rhesus The normal PCV at birth is 45–65% and the
haemolytic disease. Hb 15–25 g/dl. After delivery the PCV and
NOTE The following weight categories are a useful Hb in term infants falls steadily until about
guide to the need for an exchange transfusion: 8 weeks of age and then slowly increases. The
PCV should not fall below 35% and the Hb
Below 1500 g 1500–1999 g below 12 g/dl in a term infant. The life span
Well infant 250 μmol/l 300 μmol/l of the red cell in the infant is only 90 days
Sick infant or 200 μmol/l 250 μmol/l (3 months) compared to 120 days in the adult.
infant with
haemolysis It is important that the PCV or Hb is measured
on a sample of venous or arterial blood, or
2000–2499 g 2500 g blood collected from a warm heel. Capillary
blood sampled from a cold heel will give a
Well infant 350 μmol/l 400 μmol/l
falsely high reading.
Sick infant or 300 μmol/l 350 μmol/l
infant with NOTE Anaemia (which is diagnosed technically)
haemolysis is not the same as pallor (the clinical sign of pale
skin, nail beds and mucous membranes). While
All infants who may need an exchange anaemic infants are pale, there are many other
transfusion must be transferred urgently to a causes of pallor (e.g. cold or shock).
hospital with the staff and equipment needed.
Send parental consent and a tube of clotted
maternal blood with the infant for cross-
12. 174 NEWBORN CARE
9-32 What are the common causes of Packed cells should be given to an infant with
anaemia in the infant? anaemia of prematurity if the PCV falls below
25% or the Hb below 8.5 g/dl. An earlier
1. Anaemia of prematurity
transfusion is indicated if the PCV is below
2. Repeated removal of small volumes of blood
30% or the Hb below 10 g/dl and the infant
for special investigations(e.g. blood gases)
develops respiratory distress, signs of heart
3. Haemolytic disease of the newborn
failure or patent ductus arteriosus, fails to
4. Haemorrhage before delivery (fetomaternal
grow or has severe infection.
haemorrhage)
5. Haemorrhage at or after delivery (e.g. The packed cells must be fully cross-matched
bleeding from the umbilical cord) with the infant. Usually 10 ml/kg are given
6. Infection (e.g. septicaemia and syphilis). over 4 hours. Very small infants may need
a number of transfusions during the first
Iron deficiency is a very rare cause of anaemia
few months of life before their PCV and Hb
in the newborn period. However, iron
returns to normal spontaneously. The PCV
deficiency anaemia is common after 3 months
should be checked a week after the transfusion.
of age especially in preterm infants who have
their umbilical cord clamped immediately
after delivery and do not receive regular iron
supplements. POLYCYTHAEMIA
9-33 What is anaemia of prematurity? 9-35 What is polycythaemia?
The PCV and Hb of the preterm infant are Polycythaemia (too many red blood cells) is
normal at birth but fall faster and to a lower defined as a packed cell volume above 65% or
level than those in the term infant. The more a haemoglobin concentration above 25 g/dl. It
preterm the infant the faster and lower will is important that the blood is venous, arterial,
be the fall in PCV and Hb. In most preterm or capillary blood from a warm foot.
infants the PCV falls to 30% and the Hb to
10 g/dl. A Hb or PCV below these levels is Polycythaemic infants appear very red
common, especially in very preterm infants, (plethoric). Usually polycythaemia causes
and is called ‘anaemia of prematurity’. Anaemia no major problems although the infant may
of prematurity is often made worse by repeated become jaundiced. However, if the PCV and
blood sampling. Oral iron supplements do not Hb are very high, the blood becomes thick and
prevent or correct anaemia of prematurity. sticky causing neurological signs, respiratory
distress, hypoglycaemia and heart failure.
NOTE The cause of anaemia of prematurity is failure
of the immature kidney to secrete erythropoeitin
when the PCV and Hb fall below the normal range. 9-36 What are the causes of polycythaemia
As a result the bone marrow is not stimulated and in infants?
does not release red cells into the blood stream.
1. Chronic fetal hypoxia which is common in:
• Underweight for gestational age infants
9-34 When should you treat anaemia in the • Wasted infants
newborn infant? 2. Maternal diabetes
An infant should be transfused with packed 3. Overtransfusion:
cells if the PCV is below 45% or the Hb below • Transfusion of blood from one identical
15 g/dl at birth or during the first 24 hours. twin to the other before delivery via a
Thereafter, term infants are usually considered monochorionic placenta (twin-to-twin
for transfusion at a PCV below 30% or a Hb transfusion)
below 10 g/dl. • Accidental overtransfusion with blood
after delivery. This can occur if the
13. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 175
infant is held at a level far below the 3. Does this infant have hyperbili-
mother (placenta) before the umbilical rubinaemia? Give reasons for your answer.
cord is clamped.
No, this infant does not have hyperbili-
rubinaemia because the TSB falls within the
9-37 What is the treatment of normal range for a 3 day old infant.
polycythaemia?
If the polycythaemia causes no clinical problem 4. What is the correct management of this
it does not need to be treated. During the first infant?
few weeks the PCV and Hb gradually return to
The infant should be managed as for a healthy,
normal. However, if the infant has neurological
normal infant except that the TSB should be
signs (very jittery, convulsions or feeds poorly),
repeated daily until it starts to fall.
respiratory distress, hypoglycaemia or heart
failure due to the polycythaemia, then it
must be treated by partial plasma exchange 5. Should this infant receive phototherapy?
transfusion. The method is the same as an No. There is no reason for phototherapy.
exchange transfusion for jaundice except
that the infant is given normal saline, fresh 6. Should the mother stop breastfeeding?
frozen plasma or stabilised human serum. The
exchange is limited to 20 ml/kg. No. she should continue to breastfeed.
Although breastfeeding may result in a slightly
higher TSB, it is not necessary to stop breast-
CASE STUDY 1 feeding.
A well, breastfed, term infant develops
jaundice on day 3 and the TSB (total serum CASE STUDY 2
bilirubin) is 120 μmol/l. Both the mother
and infant are blood group 0+ve. The infant's An infant scores at 32 weeks and weighs
packed cell volume is 60% (haemoglobin 20 1600 g at birth. The infant has bilateral
g/dl) and the Coomb's test is negative. cephalhaematomas and becomes jaundiced on
day 2 with a TSB of 190 μmol/l. No treatment
1. What is the probable cause of this is given. On day 5 the infant becomes lethargic
infant’s jaundice? and hypotonic with a weak cry. The TSB is
now 370 μmol/l.
This infant probably has physiological
jaundice caused by the normally high bilirubin 1. Why do you think this infant became
production, slow bilirubin conjugation by the jaundiced?
liver, and increased bilirubin reabsorption by
the intestines. Because the infant was born preterm and has
an immature liver with slow conjugation of
2. Why does the infant not have jaundice bilirubin. In addition there is an increased
caused by ABO or Rhesus haemolytic production of bilirubin by the breakdown of
disease? haemoglobin in the cephalhaematomas.
Because both the mother and infant have the 2. How should this infant have been
same ABO blood groups and are both Rhesus treated on day 2?
positive, the infant’s Coomb’s test is negative,
and the PCV (Hb) is normal. With haemolytic Phototherapy should have been started as soon
disease, the TSB would probably be much as the TSB was above the phototherapy line.
higher and the PCV low.
14. 176 NEWBORN CARE
3. Why should you be worried if a jaundiced 4. When should the phototherapy be
infant becomes lethargic and hypotonic stopped?
with a weak cry?
When the TSB has been below the photo-
Because these are early signs of bilirubin therapy line for 24 hours. Thereafter, the TSB
encephalopathy. Remember that they may should still be monitored for a few days as the
also be early signs of other problems such as TSB may increase again due to continuing
septicaemia. haemolysis.
4. How would you treat this infant’s
hyperbilirubinaemia? CASE STUDY 4
The TSB is so high that the infant must be
given an exchange transfusion as soon as A preterm infant who weighed 1200 g at birth
possible. In the meantime, phototherapy is now a month old. For the past week the
must be started. Do not drain the cephal- infant has not gained weight but otherwise
haematomas. appears to be well. The PCV is 22%. The infant
is being treated with iron supplements. As the
infant now weights 1800 g, the mother wants
CASE STUDY 3 to take him home.
1. Does this infant have anaemia?
A term infant becomes jaundiced at 12 hours.
The mother is blood group O+ve and the Yes, because the PCV is below 30%.
infant is blood group B+. Phototherapy is
started and after 24 hours the infant no longer 2. What is your diagnosis?
appears jaundiced.
Anaemia of prematurity. Many preterm infants
fail to produce red cells for a few weeks after
1. What is the likely cause of this infant’s
birth.
jaundice?
Haemolytic disease as the jaundice was 3. How should this infant be treated?
noticed within the first 24 hours. The blood
groups suggest ABO haemolytic disease (i.e. The infant needs a transfusion with packed
mother group O and infant blood group B). cells. Normally, 10 ml/kg of blood is given over
A positive Coomb’s test would confirm the 4 hours.
diagnosis of haemolytic disease.
4. Why should this infant not be taken
2. What investigation is needed? home yet?
The infant’s TSB must be measured. Because the PCV (and Hb) may still continue
to fall. Once the infant has been transfused
he can be discharged. He should be brought
3. Do you think that the phototherapy can
back to the clinic or hospital to have his PCV
be stopped safely on day 2 as the jaundice
checked after a week.
had cleared? Explain your answer.
No. Phototherapy may clear the jaundice 5. Should this infant receive iron
although the TSB remains high. supplements?
Yes. Iron supplements will help to prevent iron
deficiency in a few months time. However,
15. JAUNDICE , ANAEMIA AND POLYC YTHAEMIA 177
340
320
300
280
Micro mol/L TSB (total serum bilirubin)
260
240
220
200
180
160
140
120
100 38+ wks or 3000+ g
35–37w 6d or 2500–2999 g
80 34–34w 6d or 2000–2499 g
60 32–33w 6d or 1500–1999 g
30–31w 6d or 1250–1499 g
40 28–29w 6d or 1000–1249 g
20 < 28w or < 1000 g
0
6h 12h 24h 36h 48h 60h 72h 84h 96h 108h120h
Time (age of baby in hours)
Figure 9-2: Detailed phototherapy chart for infants in different birth weight and gestational age categories
(e.g. 34 to 34 weeks and 6 days or 34 to less than 35 weeks). (From: A R Horn: Neonatal Medicine, University of
Cape Town.) Start intensive phototherapy when the TSB is above the line according to gestation or weight.
iron supplements will not prevent or correct 2. What is a normal PCV at birth?
the anaemia of prematurity.
At birth the normal PCV is 45 to 65%. During
the first few weeks the PCV gradually drops.
CASE STUDY 5 3. What precautions should be taken if a
sample of capillary blood is collected for a
A term infants is born at home and then taken PCV?
to the nearest hospital. On examination the
infant appears well but is noted to be very The heel must be warm and should not be
plethoric. A capillary sample of blood is taken. squeezed. Otherwise the PCV result will be
The PCV is 70%. falsely high.
1. What is the diagnosis? 4. How should this infant be managed?
The infant has polycythaemia. This is As the infant appears well there is no special
suggested clinically by the red colour and treatment needed. However, the infant should
confirmed by the high PVC. be observed for jaundice.