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ASPHYXIA/ BIRTH
ASPHYXIA
OUTLINE
INTRODUCTION/OVERVIEW
EPIDEMIOLOGY
PREDISPOSING FACTORS
AETIOPATHOGENESIS
CLINICAL MANIFESTATION
COMPLICATIONS
NEUROLOGICAL COMPLICATIONS
RENAL COMPLICATIONS
PREVENTION
SUMMARY
CONCLUSION
REFERENCES 2
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
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INTRODUCTION
Currently, birth asphyxia is graded into 3 categories
(mild, moderate and severe) using the APGAR SCORE
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DEFINITION
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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.
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PREDISPOSING FACTORS
Maternal Fetal Delivery
Hypotension Multiple gestation Cord accidents
Hypertension Congenital PROM
malformation
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
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AETIOPATHOGENESI
S
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
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AETIOPATHOGENESI
S Interference to cerebral blood flow
(hypotension, failure of autoregulation)
Hypoxia
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EARLY COMPLICATIONS
LATE COMPLICATIONS
Developmental delay
Cerebral palsy
Mental retardation
Microcephaly
Behavioral
abnormalities
Seizure disorders
(epilepsy)
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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
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CLINICAL PRESENTATION
CLINICAL PRESENTATION
Long term Sequelae
Cognitive delay
Cerebral palsy,
Dystonia
Seizure disorder
Ataxia,
Bulbar or pseudo-bulbar palsy.
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MANAGEMENT
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
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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)
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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
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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
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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
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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)
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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
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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)
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CLINICAL PRESENTATION
History and clinical features of asphyxia
Non-voiding of urine within 24 hours
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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, 29
INVESTIGATIONS
Ultrasound (selected cases):
abnormalities of renal structural or parenchyma
renal tracts including bladder size
Doppler assessment of renal vasculature
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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 31
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.
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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
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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
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management
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.
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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
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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