BIRTH ASPHYXIA

BIRTH ASPHYXIA

Birth asphyxia or hypoxia- ischemia:

It refers to a signs & symptoms of hypoxia which means poor oxygen delivery to body organs.

*hypoxemia: which refers to an arterial oxygen concentration of less

than normal.

and if hypoxemia 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.


Hypoxemia

Ischemia

Tissue anoxia

After an episode of hypoxia an anaerobic metabolism occurs and generates increased amounts of lactate and inorganic phosphates.


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 (prenatal) 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.

Causes of asphyxia during delivery:-

- Premature placental separation.
- Inadequate relaxation of the uterus to permit placental filling as 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.


- 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.

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, having low APGAR scoring. During the ensuing hours, they may remain hypotonic or change from a hypotonic to a hypertonic state, or their tone may appear normal.


Pallor, cyanosis, apnea, a slow heart rate, and unresponsiveness to stimulation are also signs of HIE.

Cerebral edema may develop during the next 24 hr and result in profound brainstem depression. During this time, seizure activity may occur; it may be severe and refractory to the usual doses of anticonvulsants. Though most often a result of the HIE, seizures in asphyxiated newborns may also be due to hypocalcemia, hypoglycemia, or infection.

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

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

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 cortical necrosis

adrenal adrenal hemorrhage

GIT perforation, ulceration, necrosis

metabolic inappropriate ADH secretion,
hyponatremia, hypoglycemia,
hypocalcemia, myoglobinuria.

Skin subcutaneous fat necrosis

blood DIC