ENCEFALOPATIA HIPOXICA ISQUEMICA NEONATAL PDF

tratamiento de la encefalopatía hipóxica isquémica posterior a la asfixia [ ] . severity of hypoxic-ischaemic encephalopathy, and frequency of neonatal [ ]. Palavras-chave: recém-nascido, asfixia perinatal, encefalopatia hipoxica- isquêmica Neonatal and perinatal mortality: country, regional and global estimates. Hypoxic-ischemic encephalopathy in adults and older children (i.e. not neonates) , also known as global hypoxic-ischemic injury, is seen in many settings and.

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For a discussion of neonatal hypoxia, refer to neonatal hypoxic-ischemic encephalopathy. Hypoxic-ischemic cerebral injury occurs at any age, although the etiology is significantly different:. They are usually intubated and have a history of prolonged resuscitation. Severe global hypoxic-ischemic injury in this population primarily affects the grey matter structures:.

encefalopaita The predominance of grey matter injury is due to its high metabolic requirement for oxygen and glucose to supply a large number of synapses. This makes grey matter more susceptible to hypoxic-ischemic injury 1.

El modelo de encefalopatía isquémica hipóxica de la isquemia perinatal

It also contains most of the dendrites where postsynaptic glutamate receptors are located. They are therefore the sites most hipozica to the effects of glutamate excitotoxicity i. Neurologic injury is caused by hypoxia neonata, to carbon monoxide toxicity, near drowning, etc. There are often secondary effects of hypoxia on cardiac myocytes, causing reduced cardiac output and causing further secondary neurological injury. Hypoxia alone rarely causes significant brain damage unless it is profound and prolonged.

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Although cerebellar injury can be seen in neonates, it tends to be more common in older patients. The reason for this predilection is not entirely clear, but it has been suggested that the relative immaturity of Purkinje cells which are normally exquisitely sensitive to ischemic damage in neonates somehow protects the cerebellar cortex 1.

Both the reversal sign and the white cerebellum sign indicate severe injury and a poor neurologic outcome 1,3. Diffusion-weighted MR imaging is the earliest imaging modality to become positive, usually within the first few hours gipoxica a hypoxic-ischemic event due to early cytotoxic edema.

During the encefalopati 24 hours, there may be restricted diffusion in the cerebellar hemispheres, basal gangliaor cerebral cortex in particular, the perirolandic and occipital cortices 1,3. The thalami, brainstem or hippocampi may also be involved. Diffusion-weighted imaging abnormalities usually pseudo-normalize by the end of the 1 st week 1.

As in younger patients, conventional T1 and T2 weighted images are often normal or demonstrate only very subtle abnormalities. In the early subacute period 24 hours to 2 weeksconventional T2 weighted images typically become positive and show increased signal intensity and swelling of the injured grey matter structures 1.

T1 hyperintensities indicating cortical laminar necrosis become evident after two weeks. This hyperintense signal does not represent hemorrhage, and it is believed to be caused by the accumulation of denatured proteins in dying cells.

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The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia | Protocol (Translated to Spanish)

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Edit article Share article View revision history. Synonyms or Alternate Spellings: Hypoxic-ischaemic encephalopathy Global hypoxic-ischaemic injury Hypoxic-ischemic injury in older children and adults hypoxic-ischemic brain injury hypoxic brain damage Hypoxic-ischaemic injury in children and adults Hypoxic-ischemic brain damage Hypoxic-ischaemic brain damage.

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