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Neonatal Emergencies
Natangwe Shimhanda
MBChB V
19/07/16
Introduction
• A rapid clinical assessment of the seriously ill neonate will
identify if there is potential respiratory, circulatory or
neurological failure. Not to exceed a minute.
• Resuscitation is given immediately, if necessary, followed by
secondary assessment and other emergency treatment.
• The neonate may present with shock, respiratory distress,
as a drowsy/unconscious or fiting child or with a surgical
emergency.
• The key to successful outcome is in the early recognition
and active management of conditions that are life-
threatening and potentially reversible.
Vital signs
Heart rate 110 - 150
Respiratory rate <60
SpO2 > 85%
Capillary refill < 2 secs
Causes
Causes cont..
Hypoglycemia
• Blood glucose < 2.6 mmol/L
Management
<72 hours
>72 hours
Milk Feeds (start early and regularly)
[Unless nil per Os], Monitor Glucose
IV glucose infusion
Repeat Blood glucose
>2.6mmol/L
*wean Glucose PRN
*increase feeds
*Repeat Blood glucose (1-
3 hourly)
*Bolus 2ml/kg 10% Dextrose water
as required
*Continuous infusion (Pump) start
6-8mg glucose/kg/min, increase by
2mg/kg/min every 30mins until
blood glucose > 2.5
*Maximum 15mg/kg/min.
*Start glucagon infusion when 10mg
gluscose/kg/min is reached
Repeat Blood glucose
Blood Glucose <2.6mmol/L
Glucagon 1-2mg/kg/24hours IV
continuous
*steroids Hydrocortisone and
Prednisolone
*Persistent Hyperinsulinemia
Diazoside 5-10mg/kg/day or
somatostatin analogue
Special Investigations
Symptomatic/ Persistent hypoglycemia
• Insulin, cortisol, Growth
Hormone
• Acid base balance
• Urine reducing
substances, ketones
• Monitor Glucose levels
(every 30 mins until
normal and then 1-3
hourly)
• As for <72 hours
• Lactate, pyruvate
• Amino acids
• others
< 72 hours
> 72 hours
Hyperglycemia
• Suspected in Neonates with a blood sugar
levels of >11mmol/L
• Possible causes:
 Iatrogenic, IV glucose infusions, steroid administration,
aminophylline, TPN (lipids)
 Very low birth weight neonate
 Sepsis
 Intra-ventricular Hemorrhage
 Stress: Asphyxia, Respiratory distress, surgery
 Transient neonatal Diabetes mellitus
Dangers and Management
• Hyper-osmolarity, osmotic diuresis, dehydration, Intracranial hemorrhage,
death
• Management:
 Confirm with blood glucose test
 Find the cause and correct
 If Administering IV fluids with 10% dextrose (neonatalyte/neolyte) switch
to 5% dextrose with 0.2 NaCl IV solution.
 Repeat blood glucose hourly and aim to keep between 5.5-11mmol/L
 If it remains above 14mmol/L in spite of limiting glucose intake to
4mg/kg/min, consider insulin therapy with consultation w/ the consultant
and preferably in an ICU setting
 Actrapid (short acting), add 1 U(0.01ml) insulin to a syringe containing
10mls 5% dextrose water
Shock
• Circulation is inadequate to meet the demands of the tissues.
• Critically ill neonates are often in shock, usually because of hypovolaemia
due to fluid loss or maldistribution of fluid, as occurs in sepsis or intestinal
obstruction
• Children normally require a much higher fluid intake per kilogram of body
weight than adults because they have a higher surface area to volume
ratio and a higher basal metabolic rate.
• Therefore they may become dehydrated if: there is loss of the normal
fluid-retaining mechanisms, e.g. the permeable skin of premature infants,
increased urinary losses or capillary leak, additional fluid losses due to
fever, diarrhoea or increased insensible losses (e.g. increased sweating or
tachypnoea)
Clinical signs
• In early, compensated shock, the BP is maintained by increased heart and
respiratory rate, redistribution of blood from venous reserve volume and
diversion of blood flow from non-essential tissues such as the skin in the
peripheries, which become cold, to the vital organs like brain and heart.
Management
• Fluid resuscitation - Rapid restoration of the
intravascular circulating volume is the priority.
Deficit: % dehydration *
weight*10
Maintenance:
First 10kg - 4ml/kg
Second 10kg – 2ml/kg
Subsequent – 1ml/kg
Ongoing losses:
5mls/kg Vomiting
10mls/kg loose stool
Subsequent management
• If there is no improvement following fluid resuscitation
or there is progression of shock and respiratory failure,
a paediatric intensive care unit should be involved and
transfer arranged as the child may need:
 tracheal intubation and mechanical ventilation
 invasive monitoring of blood pressure
 inotropic support
 correction of haematological, biochemical and
metabolic derangements
 support for renal or liver failure.
Septicaemia
• Proliferation/dissemination of bacteria in the
bloodstream, leading to the host response of
inflammatory cytokines release and activation
of endothelial cells, which may lead to septic
shock
• In neonates, the commonest causes of
septicaemia are group B streptococcus or
Gram negative organisms acquired from the
birth canal
Clinical features of Septicaemia
Management Priorities
• Antibiotics
• Fluids
 Significant hypovolaemia is often present, owing to fluid
maldistribution, which occurs due to the release of vasoactive
mediators by host inflammatory and endothelial cells. There is loss
of intravascular proteins and fluid which may occur due to the
development of ‘capillary leak’ caused by endothelial cell
dysfunction. Circulating plasma volume is lost into the interstitial
fluid
Gram Positive e.g. Group B,
Beta Hemolytic Strept and
Listeria
Gram Negative e.g. E.coli,
klebsiella, Proteus etc
Ampicillin 50-100mg/kg/24hours IV (100-
200mg/kg meningitis)
Gentamycin 5mg/kg IV
Management
Circulatory support
• Myocardial dysfunction occurs as inflammatory cytokines and
circulating toxins depress myocardial contractility. Inotropic
support may be required.
Disseminated intravascular coagulation (DIC)
• Abnormal blood clotting causes widespread microvascular
thrombosis and consumption of clotting factors. If bleeding
occurs, clotting derangement should be corrected with fresh
frozen plasma and platelet transfusions.
Steroids
• There is no evidence that steroids are of benefit in septic
shock
CNS
Signs and Symptoms
• seizures
• lethargy
• irritability/tremors
• hypotonia
Evaluation
• LP
• EEG
• US
• CT/MRI
Conditions
• Hypoxic-Ischemic
Encephalopathy (HIE)
• Intra-cranial
Hemorrhage
• Drug withdrawal
• Malformations
• Meningitis
Seizures
• Seizures occurring during the neonatal period are often
difficult to recognize.
• The cortical development is not complete, and as a
result, generalized motor activity is less common.
• Subtle seizures in the term neonate can include
abnormal eye movements (usually horizontal,
sustained eye deviation), lip smacking, abnormal
• tongue movements, pedaling, or apnea.
Classifications
• Clonic seizures
These movements most commonly are associated
with electrographic seizures.
They often involve 1 extremity or 1 side of the
body.
The rhythm of the clonic movements is usually
slow, at 1-3 movements per second.
Classifications
• Tonic seizures
 These may involve 1 extremity or the whole body. Focal
tonic seizures involving 1 extremity often are associated
with electrographic seizures.
 Generalized tonic seizures often manifest with tonic
extension of the upper and lower limbs and also may
involve the axial musculature in an opisthotonic fashion.
 Generalized tonic seizures mimic decorticate posturing; the
majority are not associated with electrographic seizures.
Classifications
• Myoclonic seizures
 These may occur focally in 1 extremity or in several
body parts (in which case they are described as
multifocal myoclonic seizures).
 Focal and multifocal myoclonic seizures typically are
not associated with electrographic correlates.
 Generalized myoclonic jerks are possibly the clinical
equivalent of infantile spasms.
Causes
Within first 24 hours of life
• Hypoxic ischemic encephalopathy
• Meningitis/sepsis
• Subdural/Subarachnoid/
Interventricular hemorrhage
• Intrauterine infection
• Trauma
• Pyridoxine dependency
• Drug effect/withdrawal
24-72 hours
• Meningitis/sepsis
• In premature infants: IVH
• In full-term infants:
infarction, venous
thrombosis
• Cerebral dysgenesis
72 hours to 1 week
• Above causes
• Inborn errors of metabolism
• Hypocalcemia
• Familial neonatal seizures
1 week to 4 weeks
Above causes
HSV
Acute Management of Neonatal
Seizures
• ABCDextrose (check HGT)
With hypoglycaemia: Glucose 10% 5ml/kg, 25 % 2-3ml/kg IV
W/out hypoglycaemia
• Phenobarbital: 20mg/kg IV loading dose; additional phenobarbital 5mg/kg IV to a
max of 20mg/kg
• Asphyxiated birth; Phenytoin 20mg/kg IV (1 mg/kg/min), Lorazepam: 0.05-0.10
mg/kg, IV
• If status epilepticus: Anaesthetic drugs and ventilate
• Hypocalcemia: Calcium gluconate, 5 % solution, 4 ml/kg IV
• Hypomagnesemia: Magnesium sulfate, 50% solution, 0.2ml/kg IM
• Pyridoxine deficiency: Pyridoxine 50-100 mg IV
Infections/Sepsis
• Ampicillin 50 mg/kg BD IV
• Gentamicin 5 mg/kg OD IV
• Meningitis- High dose Ampicillin 100mg/kg BD IV
Treatment of Electroclinical Seizures
• Phenobarbital 20 mg/kg
10 mg/kg boluses until 40-50 microgm/ml
• Phenytoin 20 mg/kg
• Lorazepam 0.1 mg/kg
• Pyridoxine 50-100 mg IV with EEG
Respiratory System
Signs and Symptoms
• tachypnea
• nasal flaring
• grunting
• retractions
• apnea
Conditions – anatomic approach
Alveolar
Hyaline Membrane Disease
(HMD) or Respiratory
Distress Syndrome (RDS)
Pneumonia
Meconium Aspiration
Syndrome (MAS)
Milk aspiration
Parenchymal
Transient Tachypnea of the
Newborn (TTN)
Cystic Adenomatoid
Malformation
Congenital Lobar
Emphysema
Space-occupying
Air Leak
Effusion
Congenital Diaphragmatic
Hernia
Airway
Laryngomalacia/tracheom
alacia
Tracheal web
Vocal cord paralysis
Choanal atresia
Extra-pulmonary
Sepsis/meningitis
Congenital Heart
Disease
Hypothermia
Metabolic error
Abdominal distention
Hyaline Membrane Disease
Meconium Aspiration Syndrome
Cystic Adenomatoid Malformation
Respiratory Distress Syndrome
Pulmonary and Extra-pulmonary Causes
Signs of respiratory distress:
• tachypnoea (>60 breaths/min)
• laboured breathing, with chest wall recession (particularly sternal and subcostal
indrawing) and nasal flaring
• expiratory grunting
• cyanosis if severe.
Affected infants should be admitted to the neonatal
unit for monitoring of heart and respiratory rates, oxygenation
and circulation. A chest X-ray will be required
to help identify the cause, especially those causes
which may need immediate treatment, e.g. pneumothorax
or diaphragmatic hernia. Additional ambient
oxygen, mechanical ventilation and circulatory support
are given as required.
Management
• Affected infants should be admitted to the
neonatal unit for monitoring of heart and
respiratory rates, oxygenation and circulation.
• A chest X-ray will be required to help identify the
cause, especially those causes which may need
immediate treatment, e.g. pneumothorax or
diaphragmatic hernia.
• Additional ambient oxygen, mechanical
ventilation and circulatory support are given as
required.
Cardiovascular System
• Congenital heart diseases (CHD) encompass a
spectrum of structural abnormalities of the
heart or intra-thoracic vessels.
• Commonly presents in the newborn with
central cyanosis, heart failure, sudden collapse
or heart murmur.
• Cyanotic or Acyanotic
Cyanotic Heart Lesions
• Cyanosis is a pathologic process caused by
deoxygenated blood in the capillary vessels.
• Cyanotic heart defects are not detected in the
newborn nursery, presents during the first 2 to 3
weeks of life when the Ductus Arteriosus closes .
• There is still adequate oxygenated blood to the
systemic circulation through a patent DA
Terrible Ts
Classically present with cyanosis
1. Transposition of the great vessels
2. Total anomalous pulmonary venous return
3. Tetralogy of Fallot
4. Truncus arteriosus
5. Tricuspid atresia
Acyanotic Heart Disease
• Acyanotic heart diseases may also be a result of
closure of the ductus arteriosus (DA).
• The onset of symptoms typically is gradual, with
the onset of congestive heart failure.
• Different degrees of obstruction to the left
ventricular outflow tract are present that result in
an increase in pulmonary blood flow and a
gradual development of heart failure.
Signs and Symptoms
• Tachypnea
• Tachycardia
• Hepatomegaly
• History of poor feeding
• Sweating or color change with feedings
• Poor weight gain
• Lower extremity edema and jugular venous
distention are unlikely findings at this age
Classic Hyperoxia Test
• Differentiate between cardiac and noncardiac causes
• Provide 100% oxygen
• Observe the oxygen saturation on pulse oximetry for
an increase of 10% in pulmonary causes (PaO2 should
increase by 30 mm Hg)
• If the neonate’s oxygen saturation or PaO2 fail to
improve, cyanotic heart disease is suspected.
Management
• Administration of prostaglandin E1 (PGE1) as a bolus of
0.05 mcg/kg IV
• Success is less likely because the development of heart
failure is gradual and the DA may already have been closed
for several days to weeks.
• First line -Furosemide, 1 mg/kg IV
• Other adjuvants include dopamine, dobutamine, and
digoxin.
• Pediatric cardiology consultation
HEMATOLOGIC
Signs and Symptoms
• Pallor
• Shock
• Early Jaundice
• Petechiae
Conditions
Acute Blood loss
• Placenta previa
• Abrutio placentae
• Velamentous cord
insertion
• Cord accident
• Organ rupture
Conditions
Chronic Blood loss
• Maternal-fetal
• Twin-twin transfusion
• Hemolytic anemias –
immune, non-immune
Conditions
• Thrombocytopenia
• Polycythemia
• Hemorrhagic Disease
of the Newborn
GASTRO-INTESTINAL SYSTEM
Conditions
• Congenital malformations
• Tracheal-Esophageal Fistula
(TEF)
• Duodenal atresia
• Intestinal atresias
• Omphalocele
• Gastroschisis
• Necrotizing Enterocolitis
(NEC)
Signs and Symptoms
• distention
• failure to stool
• vomiting
Evaluation
• Abdominal films
• Contrast studies
• US
Tracheal-Esophageal Fistula
Omphalocele
Gastroschisis
NEC - pneumotosis
Pneumotosis intestinalis
Double Bubble Sign
Intestinal atresia
Ileal Atresia
Duodenal Atresia
Congenital Diaphragmatic Hernia
Classification
Absent diaphragm : rare
Diaphragmatic hernia
• 80% posterolateral L >R
(Bochdalek)
• 2% anterior (Morgagni)
• 15 - 20% paraesophageal
Eventration (15 - 20%)
Classic Triad: Dyspnea, Cyanosis,
Apparent dextrocardia
Immediate management:
Intubation and stomach
decompression
The End
References
• Lissauer T, Clayden G, 2012. Illustrated
Textbook Of Paediatrics. Fourth edition. ©
2012 Elsevier Ltd
• Wittenberg D.F. (2009), Coovadia’s Paediatrics
and Child Health. Oxford University Press
Southern Africa (pty) Ltd
• Philip Henning, 2012. Neonatology, A Guide
For Doctors. Tygerberg Children’s Hospital,
Stellenbosch University. South Africa

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Neonatal emergencies

  • 2. Introduction • A rapid clinical assessment of the seriously ill neonate will identify if there is potential respiratory, circulatory or neurological failure. Not to exceed a minute. • Resuscitation is given immediately, if necessary, followed by secondary assessment and other emergency treatment. • The neonate may present with shock, respiratory distress, as a drowsy/unconscious or fiting child or with a surgical emergency. • The key to successful outcome is in the early recognition and active management of conditions that are life- threatening and potentially reversible.
  • 3.
  • 4. Vital signs Heart rate 110 - 150 Respiratory rate <60 SpO2 > 85% Capillary refill < 2 secs
  • 7. Hypoglycemia • Blood glucose < 2.6 mmol/L Management <72 hours >72 hours Milk Feeds (start early and regularly) [Unless nil per Os], Monitor Glucose IV glucose infusion Repeat Blood glucose >2.6mmol/L *wean Glucose PRN *increase feeds *Repeat Blood glucose (1- 3 hourly) *Bolus 2ml/kg 10% Dextrose water as required *Continuous infusion (Pump) start 6-8mg glucose/kg/min, increase by 2mg/kg/min every 30mins until blood glucose > 2.5 *Maximum 15mg/kg/min. *Start glucagon infusion when 10mg gluscose/kg/min is reached Repeat Blood glucose Blood Glucose <2.6mmol/L Glucagon 1-2mg/kg/24hours IV continuous *steroids Hydrocortisone and Prednisolone *Persistent Hyperinsulinemia Diazoside 5-10mg/kg/day or somatostatin analogue
  • 8. Special Investigations Symptomatic/ Persistent hypoglycemia • Insulin, cortisol, Growth Hormone • Acid base balance • Urine reducing substances, ketones • Monitor Glucose levels (every 30 mins until normal and then 1-3 hourly) • As for <72 hours • Lactate, pyruvate • Amino acids • others < 72 hours > 72 hours
  • 9. Hyperglycemia • Suspected in Neonates with a blood sugar levels of >11mmol/L • Possible causes:  Iatrogenic, IV glucose infusions, steroid administration, aminophylline, TPN (lipids)  Very low birth weight neonate  Sepsis  Intra-ventricular Hemorrhage  Stress: Asphyxia, Respiratory distress, surgery  Transient neonatal Diabetes mellitus
  • 10. Dangers and Management • Hyper-osmolarity, osmotic diuresis, dehydration, Intracranial hemorrhage, death • Management:  Confirm with blood glucose test  Find the cause and correct  If Administering IV fluids with 10% dextrose (neonatalyte/neolyte) switch to 5% dextrose with 0.2 NaCl IV solution.  Repeat blood glucose hourly and aim to keep between 5.5-11mmol/L  If it remains above 14mmol/L in spite of limiting glucose intake to 4mg/kg/min, consider insulin therapy with consultation w/ the consultant and preferably in an ICU setting  Actrapid (short acting), add 1 U(0.01ml) insulin to a syringe containing 10mls 5% dextrose water
  • 11. Shock • Circulation is inadequate to meet the demands of the tissues. • Critically ill neonates are often in shock, usually because of hypovolaemia due to fluid loss or maldistribution of fluid, as occurs in sepsis or intestinal obstruction • Children normally require a much higher fluid intake per kilogram of body weight than adults because they have a higher surface area to volume ratio and a higher basal metabolic rate. • Therefore they may become dehydrated if: there is loss of the normal fluid-retaining mechanisms, e.g. the permeable skin of premature infants, increased urinary losses or capillary leak, additional fluid losses due to fever, diarrhoea or increased insensible losses (e.g. increased sweating or tachypnoea)
  • 12. Clinical signs • In early, compensated shock, the BP is maintained by increased heart and respiratory rate, redistribution of blood from venous reserve volume and diversion of blood flow from non-essential tissues such as the skin in the peripheries, which become cold, to the vital organs like brain and heart.
  • 13. Management • Fluid resuscitation - Rapid restoration of the intravascular circulating volume is the priority. Deficit: % dehydration * weight*10 Maintenance: First 10kg - 4ml/kg Second 10kg – 2ml/kg Subsequent – 1ml/kg Ongoing losses: 5mls/kg Vomiting 10mls/kg loose stool
  • 14. Subsequent management • If there is no improvement following fluid resuscitation or there is progression of shock and respiratory failure, a paediatric intensive care unit should be involved and transfer arranged as the child may need:  tracheal intubation and mechanical ventilation  invasive monitoring of blood pressure  inotropic support  correction of haematological, biochemical and metabolic derangements  support for renal or liver failure.
  • 15. Septicaemia • Proliferation/dissemination of bacteria in the bloodstream, leading to the host response of inflammatory cytokines release and activation of endothelial cells, which may lead to septic shock • In neonates, the commonest causes of septicaemia are group B streptococcus or Gram negative organisms acquired from the birth canal
  • 16. Clinical features of Septicaemia
  • 17. Management Priorities • Antibiotics • Fluids  Significant hypovolaemia is often present, owing to fluid maldistribution, which occurs due to the release of vasoactive mediators by host inflammatory and endothelial cells. There is loss of intravascular proteins and fluid which may occur due to the development of ‘capillary leak’ caused by endothelial cell dysfunction. Circulating plasma volume is lost into the interstitial fluid Gram Positive e.g. Group B, Beta Hemolytic Strept and Listeria Gram Negative e.g. E.coli, klebsiella, Proteus etc Ampicillin 50-100mg/kg/24hours IV (100- 200mg/kg meningitis) Gentamycin 5mg/kg IV
  • 18. Management Circulatory support • Myocardial dysfunction occurs as inflammatory cytokines and circulating toxins depress myocardial contractility. Inotropic support may be required. Disseminated intravascular coagulation (DIC) • Abnormal blood clotting causes widespread microvascular thrombosis and consumption of clotting factors. If bleeding occurs, clotting derangement should be corrected with fresh frozen plasma and platelet transfusions. Steroids • There is no evidence that steroids are of benefit in septic shock
  • 19. CNS Signs and Symptoms • seizures • lethargy • irritability/tremors • hypotonia Evaluation • LP • EEG • US • CT/MRI Conditions • Hypoxic-Ischemic Encephalopathy (HIE) • Intra-cranial Hemorrhage • Drug withdrawal • Malformations • Meningitis
  • 20. Seizures • Seizures occurring during the neonatal period are often difficult to recognize. • The cortical development is not complete, and as a result, generalized motor activity is less common. • Subtle seizures in the term neonate can include abnormal eye movements (usually horizontal, sustained eye deviation), lip smacking, abnormal • tongue movements, pedaling, or apnea.
  • 21. Classifications • Clonic seizures These movements most commonly are associated with electrographic seizures. They often involve 1 extremity or 1 side of the body. The rhythm of the clonic movements is usually slow, at 1-3 movements per second.
  • 22. Classifications • Tonic seizures  These may involve 1 extremity or the whole body. Focal tonic seizures involving 1 extremity often are associated with electrographic seizures.  Generalized tonic seizures often manifest with tonic extension of the upper and lower limbs and also may involve the axial musculature in an opisthotonic fashion.  Generalized tonic seizures mimic decorticate posturing; the majority are not associated with electrographic seizures.
  • 23. Classifications • Myoclonic seizures  These may occur focally in 1 extremity or in several body parts (in which case they are described as multifocal myoclonic seizures).  Focal and multifocal myoclonic seizures typically are not associated with electrographic correlates.  Generalized myoclonic jerks are possibly the clinical equivalent of infantile spasms.
  • 24. Causes Within first 24 hours of life • Hypoxic ischemic encephalopathy • Meningitis/sepsis • Subdural/Subarachnoid/ Interventricular hemorrhage • Intrauterine infection • Trauma • Pyridoxine dependency • Drug effect/withdrawal 24-72 hours • Meningitis/sepsis • In premature infants: IVH • In full-term infants: infarction, venous thrombosis • Cerebral dysgenesis 72 hours to 1 week • Above causes • Inborn errors of metabolism • Hypocalcemia • Familial neonatal seizures 1 week to 4 weeks Above causes HSV
  • 25. Acute Management of Neonatal Seizures • ABCDextrose (check HGT) With hypoglycaemia: Glucose 10% 5ml/kg, 25 % 2-3ml/kg IV W/out hypoglycaemia • Phenobarbital: 20mg/kg IV loading dose; additional phenobarbital 5mg/kg IV to a max of 20mg/kg • Asphyxiated birth; Phenytoin 20mg/kg IV (1 mg/kg/min), Lorazepam: 0.05-0.10 mg/kg, IV • If status epilepticus: Anaesthetic drugs and ventilate • Hypocalcemia: Calcium gluconate, 5 % solution, 4 ml/kg IV • Hypomagnesemia: Magnesium sulfate, 50% solution, 0.2ml/kg IM • Pyridoxine deficiency: Pyridoxine 50-100 mg IV Infections/Sepsis • Ampicillin 50 mg/kg BD IV • Gentamicin 5 mg/kg OD IV • Meningitis- High dose Ampicillin 100mg/kg BD IV
  • 26. Treatment of Electroclinical Seizures • Phenobarbital 20 mg/kg 10 mg/kg boluses until 40-50 microgm/ml • Phenytoin 20 mg/kg • Lorazepam 0.1 mg/kg • Pyridoxine 50-100 mg IV with EEG
  • 27. Respiratory System Signs and Symptoms • tachypnea • nasal flaring • grunting • retractions • apnea Conditions – anatomic approach Alveolar Hyaline Membrane Disease (HMD) or Respiratory Distress Syndrome (RDS) Pneumonia Meconium Aspiration Syndrome (MAS) Milk aspiration Parenchymal Transient Tachypnea of the Newborn (TTN) Cystic Adenomatoid Malformation Congenital Lobar Emphysema
  • 28. Space-occupying Air Leak Effusion Congenital Diaphragmatic Hernia Airway Laryngomalacia/tracheom alacia Tracheal web Vocal cord paralysis Choanal atresia Extra-pulmonary Sepsis/meningitis Congenital Heart Disease Hypothermia Metabolic error Abdominal distention
  • 29. Hyaline Membrane Disease Meconium Aspiration Syndrome Cystic Adenomatoid Malformation
  • 30. Respiratory Distress Syndrome Pulmonary and Extra-pulmonary Causes Signs of respiratory distress: • tachypnoea (>60 breaths/min) • laboured breathing, with chest wall recession (particularly sternal and subcostal indrawing) and nasal flaring • expiratory grunting • cyanosis if severe. Affected infants should be admitted to the neonatal unit for monitoring of heart and respiratory rates, oxygenation and circulation. A chest X-ray will be required to help identify the cause, especially those causes which may need immediate treatment, e.g. pneumothorax or diaphragmatic hernia. Additional ambient oxygen, mechanical ventilation and circulatory support are given as required.
  • 31. Management • Affected infants should be admitted to the neonatal unit for monitoring of heart and respiratory rates, oxygenation and circulation. • A chest X-ray will be required to help identify the cause, especially those causes which may need immediate treatment, e.g. pneumothorax or diaphragmatic hernia. • Additional ambient oxygen, mechanical ventilation and circulatory support are given as required.
  • 32. Cardiovascular System • Congenital heart diseases (CHD) encompass a spectrum of structural abnormalities of the heart or intra-thoracic vessels. • Commonly presents in the newborn with central cyanosis, heart failure, sudden collapse or heart murmur. • Cyanotic or Acyanotic
  • 33. Cyanotic Heart Lesions • Cyanosis is a pathologic process caused by deoxygenated blood in the capillary vessels. • Cyanotic heart defects are not detected in the newborn nursery, presents during the first 2 to 3 weeks of life when the Ductus Arteriosus closes . • There is still adequate oxygenated blood to the systemic circulation through a patent DA
  • 34. Terrible Ts Classically present with cyanosis 1. Transposition of the great vessels 2. Total anomalous pulmonary venous return 3. Tetralogy of Fallot 4. Truncus arteriosus 5. Tricuspid atresia
  • 35. Acyanotic Heart Disease • Acyanotic heart diseases may also be a result of closure of the ductus arteriosus (DA). • The onset of symptoms typically is gradual, with the onset of congestive heart failure. • Different degrees of obstruction to the left ventricular outflow tract are present that result in an increase in pulmonary blood flow and a gradual development of heart failure.
  • 36. Signs and Symptoms • Tachypnea • Tachycardia • Hepatomegaly • History of poor feeding • Sweating or color change with feedings • Poor weight gain • Lower extremity edema and jugular venous distention are unlikely findings at this age
  • 37. Classic Hyperoxia Test • Differentiate between cardiac and noncardiac causes • Provide 100% oxygen • Observe the oxygen saturation on pulse oximetry for an increase of 10% in pulmonary causes (PaO2 should increase by 30 mm Hg) • If the neonate’s oxygen saturation or PaO2 fail to improve, cyanotic heart disease is suspected.
  • 38. Management • Administration of prostaglandin E1 (PGE1) as a bolus of 0.05 mcg/kg IV • Success is less likely because the development of heart failure is gradual and the DA may already have been closed for several days to weeks. • First line -Furosemide, 1 mg/kg IV • Other adjuvants include dopamine, dobutamine, and digoxin. • Pediatric cardiology consultation
  • 39. HEMATOLOGIC Signs and Symptoms • Pallor • Shock • Early Jaundice • Petechiae Conditions Acute Blood loss • Placenta previa • Abrutio placentae • Velamentous cord insertion • Cord accident • Organ rupture Conditions Chronic Blood loss • Maternal-fetal • Twin-twin transfusion • Hemolytic anemias – immune, non-immune Conditions • Thrombocytopenia • Polycythemia • Hemorrhagic Disease of the Newborn
  • 40. GASTRO-INTESTINAL SYSTEM Conditions • Congenital malformations • Tracheal-Esophageal Fistula (TEF) • Duodenal atresia • Intestinal atresias • Omphalocele • Gastroschisis • Necrotizing Enterocolitis (NEC) Signs and Symptoms • distention • failure to stool • vomiting Evaluation • Abdominal films • Contrast studies • US
  • 41. Tracheal-Esophageal Fistula Omphalocele Gastroschisis NEC - pneumotosis Pneumotosis intestinalis
  • 42.
  • 43. Double Bubble Sign Intestinal atresia Ileal Atresia Duodenal Atresia
  • 44. Congenital Diaphragmatic Hernia Classification Absent diaphragm : rare Diaphragmatic hernia • 80% posterolateral L >R (Bochdalek) • 2% anterior (Morgagni) • 15 - 20% paraesophageal Eventration (15 - 20%) Classic Triad: Dyspnea, Cyanosis, Apparent dextrocardia Immediate management: Intubation and stomach decompression
  • 46. References • Lissauer T, Clayden G, 2012. Illustrated Textbook Of Paediatrics. Fourth edition. © 2012 Elsevier Ltd • Wittenberg D.F. (2009), Coovadia’s Paediatrics and Child Health. Oxford University Press Southern Africa (pty) Ltd • Philip Henning, 2012. Neonatology, A Guide For Doctors. Tygerberg Children’s Hospital, Stellenbosch University. South Africa

Notas do Editor

  1. In late or uncompensated shock, compensatory mechanisms fail, blood pressure falls and lactic acidosis increases. It is important to recognise early compensated shock, as this is reversible, in contrast to uncompensated shock, which may be irreversible.
  2. 20mls/kg bolus of isotonic fluids
  3. * Do a septic screen: FBC and diff count, Blood cultures, CRP, LP, CXR, TB work up, Pus swabs, urine MCS, stool MCS
  4. Omphalocele: External herniation of abdominal viscera into the base of the umbilical cord through a central defect. Presence of covering or sac (amnion and peritoneum)
  5. Goals of Management maximize arterial oxygenation mechanical ventilation: use low inflating pressures increases pulmonary blood flow prevention of pain fentanyl infusion 3-10 mcg/kg/hr correction of acidosis