Complications of neonatal asphyxia with emphasis on brain and kidney

1. 1
EARLY NEONATAL DISEASES
RELATED TO ASPHYXIA
BY
DR. AYODELE, NOSRULLAH S
FMC, BIRNIN KEBBI

2. OUTLINE
 INTRODUCTION/OVERVIEW
 EPIDEMIOLOGY
 PREDISPOSING FACTORS
 AETIOPATHOGENESIS
 CLINICAL MANIFESTATION
 COMPLICATIONS
 NEUROLOGICAL COMPLICATIONS
 RENAL COMPLICATIONS
 PREVENTION
 SUMMARY
 CONCLUSION
 REFERENCES 2

3. INTRODUCTION
 Birth asphyxia can be defined as a clinical condition
characterised by inability/failure to initiate or sustain
spontaneous regular respiration leading to varying
degree of hypoxic and ischaemic injuries to body tissues
and organs.
 Historically categorized into two grades
 asphyxia livida (blue asphyxia) - blue appearance of the
newborn. Muscle tone is good and the infant is responsive to
stimuli
 asphyxia pallida (white/pale asphyxia) more severe, baby is
pale, flaccid and unresponsive to stimuli
3

4. INTRODUCTION
 Currently, birth asphyxia is graded into 3 categories
(mild, moderate and severe) using the APGAR SCORE 1
 According to the American College of Obstetricians and
Gynecologists and the American Academy of Pediatrics, a
neonate is labelled to be asphyxiated if the following
conditions are satisfied:
 Umbilical cord arterial pH <7
 Apgar score of 0–3 for longer than 5 min
 Neonatal neurological manifestations (e.g. seizures, coma or hypotonia);
and
 Multisystem organ dysfunction, e.g. cardiovascular, gastrointestinal,
haematological, pulmonary or renal system
4

5. INTRODUCTION
 Currently, birth asphyxia is graded into 3 categories
(mild, moderate and severe) as proposed by Sanart and
Sanart 2
 This grading depends mainly on the severity of the
clinical symptoms and signs
 Birth asphyxia can be caused by events in the
antepartum, the intrapartum or the postpartum periods
or combinations of all three.
 A recent review suggests that asphyxia is probably
primarily antepartum in 50% of cases, intrapartum in
40% and postpartum in the remaining 10% of cases 1
5

6. INTRODUCTION
 In developing countries intrapartum causes account for
a larger proportion of cases
 Poverty, ignorance, absence of standard health facilities
and trained birth attendants are impediments to the
management of birth asphyxia in Nigeria, and most
developing countries
6

7. EPIDEMIOLOGY
 According to the World Health Organization (WHO),
between 4 and 9 million newborns develop birth
asphyxia each year. 1
 About 1.2 million (23-30%) die and at least the same
number develop severe consequences, such as epilepsy,
cerebral palsy and developmental delay1
 Less than 0.1% of newborn infant deaths occur in
industrialized countries due improvements in primary
and obstetric care
7

8. PREDISPOSING FACTORS
 Any factors which interfere with the circulation
between maternal and fetal blood exchange (leading
to hypoxia) could result in the happens of perinatal
asphyxia.
 These factors can be maternal factor, fetal factor,
delivery factor or combination.
8

9. PREDISPOSING FACTORS
9
Maternal Fetal Delivery
Hypotension Multiple gestation Cord accidents
Hypertension Congenital
malformation
PROM
Diabetes Malpresentation Prolonged labour
Anaemia Preterm/prematurity Obstructed labour
Smoking Post maturity Meconium aspiration
Nephritis IUGR Oxytocin excess
Heart disease Chorioamnionitis
Extreme of age Abruptio placentae
Pre/eclampsia Placenta praevia
Drugs

10. AETIOPATHOGENESIS
 Interference with blood flow to the brain due to systemic
hypotension and a failure of autoregulation of cerebral blood
flow
 The initial circulatory response of the fetus is increased
shunting through the ductus venosus, ductus arteriosus, and
foramen ovale, with transient maintenance of perfusion of the
brain, heart, and adrenals in preference to the lungs, liver,
kidneys, and intestine (driving reflex).
 Persistence hypoxia produce ischaemia, a major factor in the
causation of brain damage.
 Ischaemia then causes neuronal and oligodendroglia damage
via excitoxicity of free radicals
10

11. AETIOPATHOGENESIS
11
Interference to cerebral blood flow
(hypotension, failure of autoregulation)
Hypoxia
Ischemia to the brain
Generation of free radicals
Reduced energy production (ATP)+ anaerobic glycolysis, lactic acidosis
Glutamate release + receptors (excitotoxic)
Change in membrane function (accumulation of Na+, NO in cells and release of Ca2+)
Cellular damage + oedema
(by affectation of mitochondrial function)

12. CLINICAL PRESENTATION
 Acidaemia, leading to an abnormal heart rate or rhythm
 Pallor
 Cyanosis
 Decreased tones and reflexes
 Poor or absent cry
 Gasping or poor respiratory effort
 Hypotonia
 Hyporeflexia
 Meconium stained liquor
 Ocular manifestation (fixed dilated pupils, nystagmus)
 Stupor
 Comma
12

13. INVESTIGATIONS
 No confirmatory test to diagnose asphyxia
 Investigations are done to assess the severity of brain injury
and to monitor the functional status of systemic organs.
 FBC
 Septic culture
 Urinalysis (ketones, ammonia)
 E/U/Cr
 Ultrasound scan
 CT – diffuse hypoattenuation
 MRI
 Electroencephalogram (EEG)
13

14. EARLY COMPLICATIONS

15. LATE COMPLICATIONS
 Developmental delay

Cerebral palsy

Mental retardation

Microcephaly

Behavioral abnormalities

Seizure disorders (epilepsy)
15

16. HYPOXIC-ISCHAEMIC
ENCEPHALOPATHY
 It is a clinical condition characterized by generalized
neurologic dysfunction emanating from hypoxic injury to
the rain tisssue
 It is an important cause of permanent damage to CNS
tissues that may result in neonatal death or manifest
later as cerebral palsy or developmental delay.4
 There are 3 clinical stages as proposed by Sarnat into
mild(HIE I), moderate (HIE II) and severe (HIE III) 2
16

17. CLINICAL PRESENTATION

19. CLINICAL PRESENTATION
 Long term Sequelae
 Cognitive delay
 Cerebral palsy,
 Dystonia
 Seizure disorder
 Ataxia,
 Bulbar or pseudo-bulbar palsy.
19

20. MANAGEMENT

21. MANAGEMENT
 Supportive therapy
 Initially NPO
 Oxygen via face mask of nasal catheter
 Assisted ventilation when required
 Correction of hypoglycaemia
 Correction of electrolyte derangement and acidosis
 Fluid restriction to prevent cerebral oedema
 ? Prophylactic antibiotics
21

22. MANAGEMENT
 Control seizure with anticonvulsants
 1st – phenbarbitone (loading 20mg/kg slowly, maintain with
5-10mg/kg/day in 2 divided doses
 If seizure persists add phenytoin (20mg/kg loading dose)
 Diazepam (0.1-0.2mg/kg) 6 hrly
 lorazepam (0.1 mg/kg)
22

23. MANAGEMENT
 Reduction of cerebral injury by induced hypothermia
 Whole body (systemic) or selective cerebral therapeutic
hypothermia reduces mortality or major neurodevelopmental
impairment in term and near-term infants.
 Decreases the rate of apoptosis and suppresses production
of neurotoxic mediators e.g. extracellular glutamate, free
radicals, nitric oxide, and lactate
 Reduces mortality and neurodevelopmental impairment if
instituted within 6 hrs
23

24. MANAGEMENT
 Isolated cerebral cooling or systemic induced servo
controlled hypothermia to a core (rectal) temperature of
33.5°C (92.3°F)
 It works by prevention of cerebral reperfusion injury by
 reduction of brain metabolism,
 suppression of inflammatory cascade,
 decreased free radical formation
 cerebral vasoconstriction thereby reducing cerebral oedema
 Agents used include antipyretics, fans, cold fluids, water filled
blanket, ice packs or cooling caps
24

25. MANAGEMENT
 Commence feeding as soon as clinical condition
improves
 Complications of induced hypothermia include
 thrombocytopenia (usually without bleeding)
 reduced heart rate, and
 subcutaneous fat necrosis
 overcooling
25

26. MANAGEMENT
 Subsequent management include
 Counselling the parents on possible developmental problems
 Management of feeding difficultiy (may need NG tube for a long
period or gastrostomy in severe case)
 Physiotherapy for limitation of disability
 Speech and language therapy (SALT)
26

27. RENAL COMPLICATIONS
 The kidneys are very sensitive to oxygen deprivation,
 Renal insufficiency may occur within 24 hours of a
hypoxic ischaemic episode
 If prolonged, may lead to irreversible cortical necrosis
 Early recognition of renal failure is important in babies
with HIE to facilitate appropriate fluid and electrolyte
management
 Diagnosis of renal failure is difficult in neonates as
many of the established clinical and biochemical
parameters are unreliable in this age group 6
27

28. RENAL COMPLICATIONS
 May be in form of acute tubular necrosis, renal vein
thrombosis and renal failure
 Acute renal failure (ARF) occurs when there is a
sudden decrease in renal function accompanied by
abnormal retention of nitrogenous wastes and serum
creatinine level rises above 1.5mg/ dL. 8
 ARF is the commonest and carries a poor prognosis
and may even result in permanent renal damage in
up to 40% of survivors
 The type of ARF following asphyxia is either pre-renal
or intrinsic renal (ATN)
28

29. CLINICAL PRESENTATION
 History and clinical features of asphyxia
 Non-voiding of urine within 24 hours
29

30. INVESTIGATIONS
 Serum biochemistry
 electrolytes, urea, creatinine, calcium, phosphate
 Urinalysis and microscopy
 haematuria , haemoglobinuria, myoglobinuria, proteinuria
 Blood
 haemoglobin (evidence of polycythaemia)
 platelet count
 pH
 base deficit or bicarbonate
 Urine biochemistry
 Creatinine, sodium, osmolality,
30

31. INVESTIGATIONS
 Ultrasound (selected cases):
 abnormalities of renal structural or parenchyma
 renal tracts including bladder size
 Doppler assessment of renal vasculature
31

32. MANAGEMENT
 Management of pre-renal failure:
 Fluid challenge with Normal Saline or Hartmann’s Solution
20mL/kg over 1 hour.
 If there is no response, intravenous 2mg to 4mg/kg of
Frusemide is given.
 Management of persistent/intrinsic failure include:
 Twice daily recording of body weight
 Fluid restriction to insensible fluid loss (20 to 30mL/kg or
400ml/m2/day) and previous day urinary output.
 This may be given as 5% or 10% Dextrose infusion or
expressed breast milk via naso-gastric tube. 8
32

33. MANAGEMENT
 Monitor serum electrolytes, BUN and Creatinine at
least daily.
 Severe hyperkalaemia is managed with
 IV Salbutamol,
 IV 10% Calcium gluconate,
 IV 8.4% Sodium Bicarbonate
 and IV Soluble insulin 0.1IU/kg with 0.5g/kg Dextrose.
 Peritoneal dialysis as a form of Renal Replacement
Therapy is indicated by life-threatening electrolytes
derangements or fluid overload.
33

34. PREVENTION
 This entails prevention of birth asphyxia and
prevention of its complications when it occurs
 Follows the five levels of prevention
1. Health education (primary)- educate the masses about it
2. Specific protection(primary)- identify risks in pregnancy and
institute preventive measures
3. Early diagnosis and treatment (secondary) – identify and
treat asphyxia promptly
4. Limitation of disability (tertiary) - physiotherapy
5. Rehabilitation (tertiary) – integration of the baby and the
mother into the community
34

35. SUMMARY
 Birth asphyxia results from inadequate oxygen supply to
the organs causing varying degrees of ischaemic injury
depending on severity
 Virtually all organs of the body are affected, worst on
the brain, kidneys, heart
 The effect can be immediate and may resolve with
appropriate management
 Long term sequalae may follow which include cerebral
palsy, seizure disorders, ental retardation and behavioral
abnormalities
 Oxygen therapy, fluid, calorie and electrolyte
management and thermal control are key in the
management
35

36. CONCLUSION
 Perinatal asphyxia remains a leading cause of infant
morbidity and mortality especially in the developing
world.
 Prompt diagnosis and appropriate management
instituted early in the disease course will help to
avert death and also give a better outcome both in
the immediate period and later in life.
36

37. REFERENCES
1. Ezeogu, Joseph. Birth Asphyxia in Nigeria; A Review.. Trop J Med Sc
and Health Research. Birth Asphyxia in Nigeria; A Review. Emechebe
GO, Ezeogu J, Odinaka KK. Trop J Med Sc and Health Research
2016:5; 6-11. 6-11.
2. Sarnat HB, Sarnat MS. Neonatal Encephalopathy Following Fetal
Distress: A Clinical and Electroencephalographic Study. Arch Neurol.
1976;33(10): 696-705.
3. Rainaldi MA, Perlman JM. Pathophysiology of birth asphyxia. Clinics
in perinatology. 2016 Sep 1;43(3):409-22.
4. Kliegman, Robert, Richard E. Behrman, and Waldo E. Nelson. Nelson
textbook of pediatrics. 20th edition (2016).
5. Mark Luscombe John C Andrzejowski. Clinical applications of induced
hypothermia. Continuing Education in Anaesthesia Critical Care &
Pain, Volume 6, Issue 1, 1 February 2006, Pages 23–27,
https://doi.org/10.1093/bjaceaccp/mki064 37

38. REFERENCES
6. Gupta BD, Sharma P, Bagla J, Parakh M, Soni JP. Renal failure in
asphyxiated neonates. Indian pediatrics. 2005 Sep 1;42(9):928.
7. Medani SA, Kheir AEM, Mohamed MB. Acute kidney injury in
asphyxiated neonates admitted to a tertiary neonatal unit in
Sudan. Sudan J Paediatr 2014; 14(2):29 - 34.
8. Ogunlesi TA, Adekanmbi F. Evaluating and managing neonatal
acute renal failure in a resource-poor setting. The Indian Journal of
Pediatrics. 2009 Mar 1;76(3):293-6.
9. Moghal NE, Embleton ND. Management of acute renal failure in the
newborn. In Seminars in Fetal and Neonatal Medicine 2006 Jun 1
(Vol. 11, No. 3, pp. 207-213). Elsevier.
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