RESUMO
The neuroimaging findings in an infant with hypernatremic dehydration are presented. Brain parenchymal haemorrhage and extensive multiple infarcts were present in the acute stage. Follow-up CT showed bilateral, symmetrical changes presumed to indicate extrapontine myelinolysis in the thalamus and globus pallidus. MRI confirmed sparing of the pons. Only three previous cases of neuroimaging abnormalities due to hypernatraemia have been described in the radiological literature.
Assuntos
Hemorragia Cerebral/etiologia , Infarto Cerebral/etiologia , Desidratação/complicações , Doenças Desmielinizantes/diagnóstico , Hipernatremia/complicações , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Hemorragia Cerebral/diagnóstico , Infarto Cerebral/diagnóstico , Doenças Desmielinizantes/diagnóstico por imagem , Humanos , Lactente , Imageamento por Ressonância Magnética , Masculino , Tomografia Computadorizada por Raios XRESUMO
Previous studies have shown that the attenuated hypoxic pulmonary vasoconstriction (HPV) of young newborn lamb lungs was enhanced by cyclooxygenase inhibition. We sought to determine whether this reflected greater synthesis of and (or) responsiveness to dilator prostaglandins (PG). Protocol 1 measured responses to graded hypoxia and perfusate concentrations of 6-keto-PGF1alpha (the stable metabolite of PGI2) and PGE2 in isolated lungs from 1-day- and 1-month-old lambs. Protocol 2 compared dose responses and segmental vascular resistances during infusion of PGI2 and PGE2 in hypoxic, cyclooxygenase-inhibited, lungs from 1- to 2-day-old and 1- to 3-month-old lambs. Lungs of 1-day-old lambs with attenuated responses to 4% O2 had significantly higher perfusate concentrations of 6-keto-PGF1alpha and PGE2, but responses to both PGE2 and the more potent vasodilator, PGI2 did not differ with age. These data support the hypothesis that attenuated HPV in young newborn lamb lungs is due to increased synthesis of dilator PG, particularly PGI2.
Assuntos
Dinoprostona/biossíntese , Epoprostenol/biossíntese , Hipóxia/metabolismo , Pulmão/metabolismo , 6-Cetoprostaglandina F1 alfa/metabolismo , Fatores Etários , Animais , Animais Recém-Nascidos , Pressão Sanguínea , Dinoprostona/metabolismo , Dinoprostona/farmacologia , Relação Dose-Resposta a Droga , Epoprostenol/metabolismo , Epoprostenol/farmacologia , Hipóxia/fisiopatologia , Técnicas In Vitro , Pulmão/crescimento & desenvolvimento , Perfusão , Artéria Pulmonar/efeitos dos fármacos , Artéria Pulmonar/fisiopatologia , Ovinos , Resistência Vascular/efeitos dos fármacos , Vasoconstritores/farmacologia , Vasodilatadores/farmacologiaRESUMO
Fulminant hepatic failure is a rare complication of status epilepticus. Although many of the anticonvulsants used to treat the seizures are known to have hepatotoxic properties, the exact mechanism leading to massive destruction of the liver following a prolonged seizure remains unclear. Three children are presented who developed fulminant hepatic failure following status epilepticus and subsequently died of multiple organ failure. The literature is reviewed with particular attention to the possible interaction between the anticonvulsants and the metabolic consequences of status epilepticus. We postulate that it is a combination of hypoxia and ischemia that occurs during a prolonged seizure with altered metabolism of free radicals secondary to the anticonvulsant drugs which leads to widespread hepatocyte membrane damage.
