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BURN ENCEPHALOPATHY

IN CHILDREN
Alia Y. Antoon, Joseph J. Volpe and John D. Crawford
1972;50;609 Pediatrics
 Neurological disturbances are common among burned patients,incidence was
14%.
 The neurological disturbances occurring in the first 48 hours to cerebral
edema developing an unidentified burn “toxin” and indicate that the majority
of these patients die.
 At autopsy, “cerebral edema” was said to be the uniform finding but no brain
weights were reported.
 Warbow and Hinton report six children with minor burns and encephalopathy
of obscure nature with two deaths and Harbauer has emphasized the
persistence of neurological deficits among survivors of burn encephalopathy.
Etiologies

Hypoxia
 Seven of the nine cases with encephabopathy due to this cause had onset of
symptoms in the first 48 hours.
 Of the two in whom symptoms developed later, one became hypoxic with
pulmonary edema
 Hypoxia developed in association with severe pneumonia due to gram-
negative organisms (Pseudomonas ) on the 61st day.
 Seven patients becoming hypoxic early in relation to smoke and carbon
monoxide inhalation.
 Rapidly progressive respiratory distress.

Hypovolemia
 Cerebral ischemia was a major cause of encephabopathy in one patient during
the “shock phase” of the burn.

Metabolic disturbances
 Hyponatremia was the etiology of encephalopathy in four of the cases.
Infection
 Septic complications leading to neurological seen in our series as early as 4 days and as late as
73 days after the injury.
 The pathological correlates included bacterial meningitis, septic microabscesses, and
microinfarcts with disseminated intravascular coagulation.

Focal lesions
 Three patients developed neurological signs late in their courses.
 The temporal evolution and discretely focal nature suggested a vascular etiology.
 In one case, a cortical vein thrombosis secondary to direct extension of inflammation from an
area of the denuded calvarium. In another case, gliosis in a cortical scar resulting from an
earlier vascubar lesion (i.e., “watershed” infarct ).
 In the third patient it was not possible to discriminate between a small embolic infarct or
cortical vein thrombosis as the abnormality underlying the focal signs.
Unknown
 One case (case 6 ) had a transient neurological disturbance with seizure
activity occurring on the ninth day.
 This was the only case in which no clear etiology was apparent.
Table
Findings

 These indicate that the neurological disturbances which occur early after a
burn injury depend principally upon hypoxia or ischemia.
 Seizures and other neurological findings developing later may have sepsis or a
metabolic aberration as the underbying basis.
 Focal neurological signs suggest abscess, infarct, or localized venous
thrombosis.
 Not seen in this series were neurological disturbances due to
hexachlorophene’5 nor have we encountered encephalopathy due to
hypertension alone or in association with hypercalcemia.
Cerebral edema

 In our pathological material, two patients had increased weight of brain and
clear evidence for brain swelling. The brain weight was increased to 1,420 gm
in comparison with the normal of 1,313 gm and contained multiple
microabscesses.
 In the second instance, brain swelling was grossly apparent with a weight of
1,420 gm in contrast to the normal of 849 gm.
 This infant had died within 24 hours of bum injury and five hours after
cardiopulmonary arrest secondary to smoke inhalation and hypoxia.
 Complete neuropathological examination was carried out in patients, whom died with severe
infection.
 One cased caused by Pseudomonas meningitis, another case caused by severe hypoxic changes
with pseudolaminar necrosis of cerebral and cerebellar cortices after dying with sepsis.
 The remaining three cases had minimal or no abnormalities of brain despite death dueto sepsis
but manifestations of infection had been evident clinically and were readily identified in other
organs pathologically.
Conclusion

Most of the reported cases “burn encephalopathy” have occurred in infants


whose syndrome began with seizures, followed by deterioration of the
neurological state and death with “cerebral edema.”