Investigação de icterícia / Investigation of jaudice

Este trabalho é uma revisão da literatura sobre como investigar a icterícia no paciente adulto. Para isso, é imprescindível entender o metabolismo da bilirrubina, a fisiopatologia da hiperbilirrubinema e reconhecer os principais diagnósticos diferenciais de icterícia no adulto.

This article is a literature review on jaundice investigation in adult patients. Therefore, it is necessary for the understanding, knowing about the metabolism of bilirubin and the pathophysiology of hyperbilirrubinemia as well as recognizing the main differential diagnoses of jaundice in adults.

Síntese e metabolismo da bilirrubina e fisiopatologia da hiperbilirrubinemia associados à Síndrome de Gilbert: revisão de literatura / Bilirubin synthesis and metabolism, and hyperbilirubinemia associated with Gilbert’s Syndrome: A review of the literature

A icterícia é sinal clínico comum a várias condições patológicas, podendo ser evidenciada em vários locais do organismo devido à grande capacidade de impregnação do pigmento biliar. A icterícia torna-se evidente quando a concentração plasmática encontra-se acima de 2,5 a 3,0 mg/dL. O presente trabalho retrata o metabolismo fisiológico dos pigmentos biliares concomitantemente com a síntese e metabolismo de bilirrubina, assim como processos fisiopatológicos causados pelo aumento da bilirrubina plasmática (hiperbilirrubinemia), como ocorre na síndrome de Gilbert, caracterizada pela deficiência enzimática, que se manifesta clinicamente como icterícia. Compreender os passos da formação e excreção da bilirrubina é fundamental para a compreensão das manifestações clínicas e que ocorrem na icterícia, facilitando o entendimento dos mecanismos fisiopatológicos da hiperbilirrubinemia, como ocorrem na síndrome de Gilbert.

Jaundice is a common clinical manifestation of several pathological conditions. It can be found in several parts of the body because of the high impregnation capacity of the bile pigment. Jaundice is evident when plasmatic concentration is higher than 2.5 ? 3.0 mg/dL. This paper describes the physiological metabolism of bile pigments concomitantly with bilirubin synthesis and metabolism, as well as the pathophysiological processes derived from increased plasmatic bilirubin (hyperbilirubinemia). This is a circumstance typical of the Gilbert?s syndrome, which causes enzymatic deficiency that is clinically manifested as jaundice. Knowledge of the steps of bilirubin formation and excretion is crucial to shed light into the clinical manifestations of jaundice and thus gain more understanding of the physiological mechanisms of hyperbilirubinema associated with Gilbert?s syndrome.

Evaluación de la audición en lactantes con alto riesgo con potenciales evocados auditivos del tallo cerebral / Evaluation of hearing in the high-risk infant with brain-stem auditory evoked potentials

Se estudiaron cuarenta niños entre 1 y 6 meses de edad, 20 con factores de alto riesgo para desarrollar hipoacusia neurosensorial adquirida postnatalmente: prematurez, hipoxia, hiperbilirrubinemia, meningitis y la utilización de aminoglucósidos; y 20 lactantes sir riesgo, que conformaron el grupo control. En ambos grupos se valoró la audición mediante potenciales evocados auditivos del tallo cerebral, con la finalidad de conocer la repercusión de estos antecedentes en la capacidad auditiva. Se midió especificamente la latencia de la onda V para definir la integridad y la madurez de la vía auditiva. Se encontró una diferencia estadísticamente significativa de p<0.01 entre el grupo de alto riesgo (6.55 +/- 0.46 en el oído derecho y 6.63 +/- 0.43 en el oído izquierdo) y el grupo control (6.31 +/- 0.29 en el oído derecho y 6.35 +/- 0.08 en el oído izquierdo). Además la administración de aminoglucósidos (80 por ciento) se relacionó con mayor frecuencia con alteraciones en los potenciales evocados. Consideramos que los potenciales evocados auditivos del tallo cerebral son necesarios en la evaluación de los infantes con alto riesgo

One year outcome of babies with severe neonatal hyperbilirubinemia and reversible abnormality in brainstem auditory evoked responses.

Brainstem auditory evoked responses (BAER) were longitudinally recorded prospectively in 18 term infants with neonatal hyperbilirubinemia (NHB) (total serum bilirubin > 15 mg/dl). Seven neonates had abnormal BAER. Wave complex IV-V was absent in eight recordings in NHB group while they were normal in the control group (p < 0.001). Prolongation of latency of waves I and V and interwave conduction time (wave I-V) occurred in jaundiced infants especially when unconjugated serum bilirubin level rose above 22 mg/dl. The abnormalities in BAER reversed to normal in all seven neonates after exchange blood transfusion indicating transient nature of bilirubin toxicity to the brain. All seven neonates in the study and control group had normal hearing, development quotient and were free of neurological sequelae on follow up for one year.

Icterícia / Jaundice

A icterícia reflete perturbaçoes no balanço entre a produçao e o "clearance" hepático da bilirrubina. Sao discutidos o metabolismo da bilirrubina e aspectos da fisiopatologia, manifestaçoes clínicas e causas da hiperbilirrubinemia. Sao abordados ainda parâmetros clínicos que devem ser valorizados na avaliaçao do paciente ictérico.

Auditory brainstem responses (ABR) in neonates with hyperbilirubinemia.

The technique of ABR testing was applied to 25 infants with neonatal hyperbilirubinemia at levels exceeding that for exchange transfusion, in an attempt to study potential influence of bilirubin toxicity on the auditory brainstem pathway. The test was performed at a mean conceptional age of 40.4 +/- 0.6 weeks just after discharge. Twenty normal term neonates of comparable birth weights and conceptional ages, who had no hyperbilirubinemia, were also examined for comparison. Fifty six percent (n = 14) of the hyperbilirubinemic neonates had some abnormality in the ABR pattern, the major one being a transient increase in the threshold of wave V (7, fail-30; 5, fail-45). Wave V, however, was consistently present at 30 dBnHL click stimulus in all the normal neonates (pass-30; normal threshold). Further, mean ABR latencies (wave III, V) and 1-V interpeak latency (brainstem conduction time) were significantly prolonged in jaundiced neonates as compared with controls (P less than 0.01). ABR changes were strongly correlated with the serum bilirubin levels (P less than 0.001). On follow up retesting at 3 months, however, all infants were found to have normal ABR latencies and threshold. Neonatal jaundice was associated with significant transient aberrations of ABR, suggestive of a transient toxic brainstem encephalopathy.