Pediatric/ BIRTH ASPHYXIA
Birth asphyxia or hypoxia- ischemia:
It refers to a signs & symptoms of hypoxia which means poor oxygen delivery to body organs that is induced by:-
*hypoxemia: which refers to an arterial oxygen
concentration of less than normal.
It refers to a signs & symptoms of hypoxia which means poor oxygen delivery to body organs that is induced by:-
*hypoxemia: which refers to an arterial oxygen
concentration of less than normal.
and if hypoxia is prolonged, cardiac and vascular
compromise occur result in hypotension causing:
* ischemia: which refers to a blood flow to cells or an
organ that is insufficient to maintain their normal
function which will result in more tissue hypoxia.
Eventually:
*Tissue anoxia occur which is a term used to indicate the
consequences of complete lack of oxygen.
* ischemia: which refers to a blood flow to cells or an
organ that is insufficient to maintain their normal
function which will result in more tissue hypoxia.
Eventually:
*Tissue anoxia occur which is a term used to indicate the
consequences of complete lack of oxygen.
Hypoxemia
Ischemia
Tissue anoxia
After an episode of hypoxia and, anaerobic metabolism occurs and generates increased amounts of lactate and inorganic phosphates.
Excitatory and toxic amino acids, particularly glutamate, accumulate in the damaged tissue.
Increased amounts of intracellular sodium and calcium may result in tissue swelling and cerebral edema. There is also increased production of free radicals and nitric oxide in these tissues.
Tissue anoxia
After an episode of hypoxia and, anaerobic metabolism occurs and generates increased amounts of lactate and inorganic phosphates.
Excitatory and toxic amino acids, particularly glutamate, accumulate in the damaged tissue.
Increased amounts of intracellular sodium and calcium may result in tissue swelling and cerebral edema. There is also increased production of free radicals and nitric oxide in these tissues.
Etiology: Hypoxia-ischemia can occur before, during or
after delivery:-
Intrauterine (before delivery) asphyxia, here there is no
sufficient gas exchange in the fetus through the placenta,
occur in the following conditions:-
Intrauterine (before delivery) asphyxia, here there is no
sufficient gas exchange in the fetus through the placenta,
occur in the following conditions:-
- interuption of the umbilical circulation as in cord prolapse.
- poor perfusion of the maternal side of the placenta as in
maternal hypotension, pre eclampsia, abruptio placentae.
- impaired maternal oxygenation as in asthma,pulmonary
embolism or pneumonia.
- impaired fetal oxygenation or perfusion as in fetomaternal
hemorrhage or fetal thrombosis.
maternal hypotension, pre eclampsia, abruptio placentae.
- impaired maternal oxygenation as in asthma,pulmonary
embolism or pneumonia.
- impaired fetal oxygenation or perfusion as in fetomaternal
hemorrhage or fetal thrombosis.
Causes of asphyxia during delivery:-
- premature placental separation.
- inadequate relaxation of the uterus to permit placental
filling as a result of uterine tetany caused by excessive use
of oxytocine during labor.
- impedence of the circulation of blood through the umbilical
cord as a result of compression or knotting of the cord.
- inadequate relaxation of the uterus to permit placental
filling as a result of uterine tetany caused by excessive use
of oxytocine during labor.
- impedence of the circulation of blood through the umbilical
cord as a result of compression or knotting of the cord.
Causes of asphyxia after birth:-
- anemia severe enough to lower the oxygen content of the
blood to a critical level due to severe hemorrhage or
hemolysis.
- shock severe enough to interfere with the transport of
oxygen to vital cells as in adrenal hemorrhage,IVH,
overwhelming infection, or massive blood loss.
- a deficit in arterial oxygen saturation resulting from failure
to breathe adequately postnatally due to a cerebral defect,
maternal medication narcosis, or injury or due to
neuromuscular disease as myasthenia gravis or myopathy.
blood to a critical level due to severe hemorrhage or
hemolysis.
- shock severe enough to interfere with the transport of
oxygen to vital cells as in adrenal hemorrhage,IVH,
overwhelming infection, or massive blood loss.
- a deficit in arterial oxygen saturation resulting from failure
to breathe adequately postnatally due to a cerebral defect,
maternal medication narcosis, or injury or due to
neuromuscular disease as myasthenia gravis or myopathy.
-failure of oxygenation of an adequate amount of blood
resulting from severe forms of cyanotic congenital heart
disease or deficient pulmonary function as hyaline membrane
disease, neonatal pneumonia, meconium aspiration,
pneumothorax, diaphragmatic hernia, pulmonary hypoplasia,
or pleural effusion.
disease or deficient pulmonary function as hyaline membrane
disease, neonatal pneumonia, meconium aspiration,
pneumothorax, diaphragmatic hernia, pulmonary hypoplasia,
or pleural effusion.
Clinical manifestations:-
Intrauterine growth restriction with increased vascular resistance may be the 1st indication of fetal hypoxia. During labor, the fetal heart rate slows. Continuous heart rate recording may reveal a variable or late deceleration pattern particularly in infants near term.
These signs should lead to the administration of high concentrations of oxygen to the mother and consideration of immediate delivery to avoid fetal death and CNS damage.
At delivery, the presence of meconium-stained amniotic fluid is evidence that fetal distress has occurred. At birth, affected infants may be depressed and may fail to breathe spontaneously. During the ensuing hours, they may remain hypotonic or change from a hypotonic to a hypertonic state, or their tone may appear normal.
These signs should lead to the administration of high concentrations of oxygen to the mother and consideration of immediate delivery to avoid fetal death and CNS damage.
At delivery, the presence of meconium-stained amniotic fluid is evidence that fetal distress has occurred. At birth, affected infants may be depressed and may fail to breathe spontaneously. During the ensuing hours, they may remain hypotonic or change from a hypotonic to a hypertonic state, or their tone may appear normal.
Signs stage 1 stage 2 stage 3
-
level of hyperalert lethargic stuporous,
consciousness coma
muscle tone normal hypotonic flaccid
posture normal flexion decerebrate
tendon hyperactive hyperactive absent
reflexes
Moro reflex strong weak absent
pupils dilated constricted unequal,poor
response to
light
seizures none common decerebration
EEG normal low voltage suppression to
changing to isoelectric line
seizur activity
duration < 24 hours 24hr - 14 days days to weeks
outcome good variable death,severe
deficits
level of hyperalert lethargic stuporous,
consciousness coma
muscle tone normal hypotonic flaccid
posture normal flexion decerebrate
tendon hyperactive hyperactive absent
reflexes
Moro reflex strong weak absent
pupils dilated constricted unequal,poor
response to
light
seizures none common decerebration
EEG normal low voltage suppression to
changing to isoelectric line
seizur activity
duration < 24 hours 24hr - 14 days days to weeks
outcome good variable death,severe
deficits
Treatment:-
Selective cerebral or whole body (systemic) therapeutic hypothermia reduces mortality or major neurodevelopmental impairment in term and near-term infants with HIE. Hypothermia decreases the rate of apoptosis and suppresses production of mediators known to be neurotoxic, including extracellular glutamate, free radicals, nitric oxide, and lactate.
Additional therapy for infants with HIE includes supportive care directed at management of organ system dysfunction. Hyperthermia has been found to be associated with impaired neurodevelopment, so it is important to prevent hyperthermia before initiation of hypothermia. Careful attention to ventilatory status and adequate oxygenation, blood pressure, hemodynamic status, acid-base balance, and possible infection is important.
Additional therapy for infants with HIE includes supportive care directed at management of organ system dysfunction. Hyperthermia has been found to be associated with impaired neurodevelopment, so it is important to prevent hyperthermia before initiation of hypothermia. Careful attention to ventilatory status and adequate oxygenation, blood pressure, hemodynamic status, acid-base balance, and possible infection is important.
Effects of asphyxia on different parts of the body
system effects
central nervous hypoxic ischemic enceohalopathy,
system infarction intracranial hemorrhage,
seizures, cerebral edema, hypotonia
hypertonia.
Cardiovascular myocardial infarction, poor
contractility tricuspid insufficiently
hypotention.
Renal acute tubular or tubular necrosis
adrenal adrenal hemorrhage
GIT perforation, ulceration, necrosis
metabolic inappropriate ADH secretion,
hyponatremia, hypoglycemia,
hypocalcemia, myoglobinuria.
Skin subcutaneous fat necrosis
blood DIC
central nervous hypoxic ischemic enceohalopathy,
system infarction intracranial hemorrhage,
seizures, cerebral edema, hypotonia
hypertonia.
Cardiovascular myocardial infarction, poor
contractility tricuspid insufficiently
hypotention.
Renal acute tubular or tubular necrosis
adrenal adrenal hemorrhage
GIT perforation, ulceration, necrosis
metabolic inappropriate ADH secretion,
hyponatremia, hypoglycemia,
hypocalcemia, myoglobinuria.
Skin subcutaneous fat necrosis
blood DIC
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