BIRTH ASPHYXIA Lec. 3 2016-2017.

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Presentation transcript:

BIRTH ASPHYXIA Lec. 3 2016-2017

Birth asphyxia or hypoxia- ischemia 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. 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.

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.

Clinical manifestations Intrauterine: IUGR with increased vascular resistance (by doppler study) 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.

Patterns of periodic fetal heart rate deceleration

After 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. Pallor Cyanosis Apnea Bradycardia Unresponsiveness to stimulation. 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.

Stages of HIE

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. Hyperthermia has been found to be associated with impaired neurodevelopment, so it is important to prevent hyperthermia before initiation of hypothermia. 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.

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