Please enable JavaScript.
Coggle requires JavaScript to display documents.
Birth Asphyxia :birthday: (:frame_with_picture: Clinical presentation…
Birth Asphyxia
:birthday:
:four_leaf_clover:
Definition
:seedling:
Asphyxia
(มาจากกรีก):
stopping of pulse
:seedling:
Perinatal asphyxia
: characterized by Impairment of exchange of Respiratory gases
➯ Hypoxemia & Hypercapnia, accompanied by metabolic acidosis
:seedling:
Hypoxemia
: diminished amount of O2 in blood supply
:seedling:
O2 deprivation
: happens during labor; affects O2 blood fr รกไปลูก
Causes including
Maternal
Fetal
Acute cord compression
Uterine rupture
Shoulder dystocia
:seedling:
Hypoxia/Anoxia
: denotes
partial
or
complete
lack of O2 respectively, in 1 or more tissues of body —including blood steam
:seedling:
Ischemia
: :arrow_down: or :no_entry: cessation of blood flow that arises fr either
systemic hypotension
,
cardiac arrest
, or occlusive vascular disease
:seedling:
Cerebral ischemia
: Dminished amount of blood perfusing the brain
:earth_americas:
Incidence
Perinatal asphyxia: ~1.5% of live births in
developed
countries
Birth asphyxia in
undeveloped
countries
Mild to moderate birth asphyxia suffered in 10% of newborn
Severe birth asphyxia suffered in 1% of newborns
:crystal_ball:
3rd M/C
cause of neonatal death (
23%
) after the Preterm birth (28%) and Severe infections (26%)
:blue_heart:
Etiology
:spades:
Antepartum
risk factors
:spades:
Intrapartum
risk factors
:waning_gibbous_moon: Criteria for a Dx
Asphyxia
ACOG def
Profound metabolic or mixed academia (pH < 7)
in an umbilical aftery blood ➯ Sample
Persistence of an Apgar score 0 to 3 for
for more than 5 mins
Neonatal neurologic abnormalities (eg. Hypotonia, Seizures)
Multiple organ involvement
(eg. Kidney, lungs, liver, hearts & intestines
Cord gas analysis
Apgar score
:gear:
PathoPSO
Starting Asphyxia ➯ fetus adapting by :arrow_up:respiratory effort & :arrow_up:BP ➯
then followed by ➯ Primary apnea ➯ :arrow_down:HR & nm BP
if asphyxia continues
➯ Fetus starts to gasp followed by ➯
Secondary apnea ( :arrow_down: HR, :arrow_down: BP, Low O2, :arrow_up: CO2, :arrow_down: pH)
Brief asphyxia
Redistribute
of CO + :arrow_up: proportion going into Brain, Heart, & Adrenal glands (
Diving reflex
- shift blood to vital organ)
Prolonged asphyxia
Cardiac func deteriorates
Hypotension
:arrow_down: Cerebral blood flow
Adequate CBF ➯ helps guiding O2 & glucose to brain ➯ maintain homeostasis & maintain cell energy
Prolonged asphyxia ➯ Loss of pressure autoregulation ➯ Disrupts Cerebral perfusion ➯ :arrow_down: Cerebral blood flow ➯ changed into using Anaerobic metabolism ➯ uses glucose :arrow_up: and small ATP is create ➯
Cellular energy failure
happens
:arrow_down:
Cerebral perfusion
:arrow_down: delivery of O2 & glucose to brain ➯ leds to
Anaerobic metabolism
:arrow_down: production of ATP ➯ affects
Na/K ATPase pump
:arrow_up: Lactic acid ➯ Tissue acidosis
Deletion in ATP ➯ :arrow_down: transcellular transport ➯ leds to Intracellular acc. of Na, H2O & Ca (influx) ➯ Tissue edema & Cerebral edema
Excitiotoxicity
Cell releases Excitatory amino a. :name_badge:
glutamate
& Calcium flows into the cell
(Excitotoxicity)
➯ induce destructive enz & free radical ➯ Damage tissue ➯ cell injury and death by Excessive glutaminergic activation
:name_badge:
glutamate
attach to its receptor ➯
Ca influx
into cell ➯ stimulate degrading enz ➯ cell ยิ่งแย่ ➯ cell damage
Peroxidation of free fatty a
O2 free radicals will peroxidase free fatty a ➯ led to more cellular damage
Production of NO can bind with Superoxide ➯ stimulate lipid peroxidation
As anaerobic metabolism produce little ATP ➯ produce more substitute energy fr
lactate, ketone, free fatty a
Culmination of Energy failure, Acidosis, Glutamate release, Lipid peroxidation, and Toxic effects of NO ➯ led to Cell death via Necrosis & Activates apoptotic cascades
:white_flower:
Features of Hypoxic-Ishcemic Encephalopathy
Depends on
Timing of injury
Degree of medical intervention
Partial recovery occurs during
30-60 min after
acute insult of primary phase of injury
Latent phase
may last fr
1-6 hrs
& characterized by
recovery of
oxidative metabolism, inflammation & continuation of Activated apoptotic cascades
Secondary phase of injury
occurs within ~
6-15 hrs after
injury
characterized by
Cytotoxic edema
Excitotoxicity
Secondary energy failure with Nearly complete failure of mitochondrial activity
Tertiary phase
occurs during
months after
Acute insult and
involes
Late cell death
Remodeling of injured brain
Astrogliosis
:zap:
Energy failure
Primary
energy failure :bear:
Asphyxia stimulates Sympathetic nervous system
Rapid depletion of Brain energy —
Anaerobic mech
Depletion of ATP
:arrow_up: lactic acid
Necrosis of neuronal cells causes Cell death
After few hrs ➯ Cerebral energy metabolism recovers
tho Cascade of biochemical events that alrdy happen
continue
Secondary
energy failure :bear:
6-15 hrs later
Brief
period of restored cellular func
Energy failure that clinically assoc. with
Seizures & Worsening neurologic exam
:arrow_down: Cerebral blood flow
Cytotoxic edema
Excitotoxic amino a (glutamate) accumulation
Mitochondrial failure :star2:
Cell necrosis & Apoptotic Death
:white_flower:
PathoPSO of HIE
:frame_with_picture:
Clinical presentation
Neurological
: Abnormal consciousness, Seizure(Transient Myocardial ischemia), Hypoxic ischemic encephalopathy
CVS
: Bradycardia, Arrhythmias, Hypotension
Respiratory
: RDS, PPHN, Pulmonary edema
GI
: :arrow_up: risk of bowel ischemia (as blood shift to supply other organs) , NEC
Kidney
: ATN, oliguria, Cr rising
Metabolic
: hypoglycemia or hyperglycemia, hypocalcemia, hyponatremia
Hemato
: DIC, poor production of clotting factors & plts
Clinical staging
:grapes:
:green_apple:
Treatment
Systemic support
:hatching_chick:
Ventilation
To maintain CO2 in normal range
Hyper
capnia ➯ Cerebral acidosis & Cerebral vasodilation
may cause ➯ blood will supply uninjured area + relative ischemic at injured area (
steal phenomenon)
Hypocapnia
➯ Low Cerebral blood flow ➯ even more ischemia
Oxygenation
To maintain O2 in normal range (PaO2 60-80)
Hyperoxia
➯ may cause :arrow_down: CBF or Exacerbate free raical Damage
should be avoided
Hypoxia
➯ Supplementarum O2 and/or Mechanical stimulation
Temperature
Always avoided Hyperthermia
Perfusion
Adequate mean systemic arterial BP for maintaining adequate Cerebral perfusion pressure
Maintain PSO metabolic state
Maintain
Ca
in normal range
HypoCa
กด Cardiac contractility & กระตุ้นให้เกิด seizure
Maintain
blood glucose
in normal range (keep 75-100 mg%)
Hypo
glycemia may➯ :arrow_up: CBF ➯ sti. Energy deficit + cause Seizure
Hyper
glycemia ➯ :arrow_up: Brain lactate, Damage to cellular integrity, Cerebral edema or Disrupt vascular autoregulation
Judicious fluid management
Should avoided Fluid overload & Inadequate circulatory volume
2 processes predispose to Fluid overload in Asphyxia