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SÍNDROME DE
LISIS TUMORAL
CUE Alexander Von Humboldt
Seminario de Pediatria
PRESENTADO POR:
Angulo Jose
Erazo Stevens
Escobar Laura
Rodriguez Santiago
2022
INTRO/DEFINICIÓN
01
HISTORIA
02
FACTORES
RIESGO
04
CLINICA Y DX
05
TABLA DE CONTENIDOS
FISIOPATOLOGÍA/
CLASIFICACIÓN
03
TTOS Y
ACTUALIZACIÓN
06
WWW.SLIDESGO.COM DISEASE
2022
DEFINICION
Lisis de células malignas, debida a apoptosis o por la acción
de la quimioterapia, se presenta la liberación rápida de
elementos intracelulares en cantidades que superan la
capacidad de excreción renal, causando alteraciones
metabólicas y disfunción orgánica.
Hiperuricemia,Hiperpotasemia,Hiperfosfatemia,
acompañadas o no de hipocalcemia e insuficiencia renal
aguda
2022
01
HISTORIA 02
2022
QUIMIOTERAPIA
1993:Garrow y
Handel
2004:Cairo y
Bishop
2011:Howard
RELEVANCIA
RELEVANCIA
FISIOPATOLOGIA
https://www.pediatriaintegral.es/publicacion-2019-03/urgencias-oncologicas-
en-pediatria/
2011
Retiro la
elevación del
25%
Hipocalcemia
sintomatica
TIPOS DE SÍNDROME DE LISIS
TUMORAL
FACTORES
DE RIESGO
04
WWW.SLIDESGO.COM DISEASE
2022
PRIMORDIAL
EL TIPO DE CA
https://slacip.org/manual-slacip/descargas/SECCION-13/13.2-
Lisis%20Tumoral-Final.pdf
https://slacip.org/manual-slacip/descargas/SECCION-13/13.2-
Lisis%20Tumoral-Final.pdf
FACTORES DE RIESGO
CANCER PRESENTACIÓN
CLÍNICA
MEDIDAS
DE
SOPORTE
LABORATORIOS
Tipo de CA
Características
del tumor
Potencial de
lisis celular
Potasio
exogeno
Fosfato
exogeno
Nefropatias
DH
Orina Acida
Hipotensión
Exposición
nefrotoxinas
LDH
Leucos
Acido urico
y calcemia
Creatinina
TFG
Cristales de
ácido úrico
Factores que
aumentan
riesgo evolución
CLINICA
05
WWW.SLIDESGO.COM DISEASE
2022
Sintomatología depende de la gravedad del trastorno hidroelectrolítico
HIPERKALEMIA
CARDIACA: arritmias, FA,
asistolia, TV, paro
NEUROMUSCULAR:
debilidad parestesias, espasmos,
parálisis flácida
HIPERFOSFATEMIA
PRECIPITACIÓN RENAL:
formación de cristales
Nitrógeno ureico y
Creatinina
HIPOCALCEMIA
CARDIOVASCULAR: hipotension,
cambios ekg
NEUROLÓGICO: tetania, alteraciones
musculares, laringoespasmos
Estado mental? -- confusion - alucinacion -
convulsion
HIPERURICEMIA
RENAL: nauseas, vomito,
oliguria, anuria, anorexia
Nitrógeno ureico y
Creatinina
TRATAMIENTO
06
1. ESTRATIFICAR
FACTORES DE RIESGO
Según el tipo de tumor y el
recuento de leucocitos
2. MONITORIZAR
3. MANEJO INICIAL
1. Hidratación IV agresiva
2. Hipouricemiantes
3. Control del K+
4. Control de fosfatos
1. ESTRATIFICAR FACTORES DE RIESGO PARA SLT
Pruebas de Laboratorio:
- Hemograma + recuento
leucocitario
- Análisis de orina
- Electrolitos
- Gases venosos
- Calcio, Fosforo, Magnesio
- Ácido úrico
- BUN
- Creatinina
- Deshidrogenasa láctica
- Pruebas hepáticas
- ECG
Imágenes
- TAC / Ecografía
2. MONITORIZAR
DIURESIS SIGNOS VITALES
MARCADORES
SÉRICOS
Cada 4 - 6 horas si hay alto riesgo de SLT
3. MANEJO INICIAL
A.HIDRATACIÓN INTRAVENOSA AGRESIVA
- ↑ Velocidad de filtrado glomerular.
- Iniciar: 24h antes de la quimioterapia; Mantener: 48h
Post quimioterapia.
Administrar:
- 2 - 3 L/m2/d.
- 200 ml/kg/d (Si <10kg)
Gasto urinario objetivo:
- ≥100ml/m2/h
- 4 - 6 ml/kg/h (Si <10kg)
Se puede adicionar Bicarbonato 40 - 60 mEq / L
3. MANEJO INICIAL
B. HIPOURICEMIANTES
Alopurinol
- Inhibidor de la xantina oxidasa
- 12 - 24h antes de la quimioterapia
- Se reserva a pacientes con riesgo bajo de
SLT
Rasburicasa
- Degrada el ácido úrico a alantoína
- Acción mas rápida (4 horas)
- Se reserva a pacientes con niveles muy
altos de ácido úrico por su alto costo.
3. MANEJO INICIAL
C. CONTROL DEL K+
- Minimizar o suspender los aportes de potasio en
los líquidos.
- Pacientes asintomáticos: Resinas
- Pacientes sintomáticos:
- Infusión de insulina + glucosa
- Gluconato de calcio
- Bicarbonato de sodio
- Nebulizaciones de salbutamol
- Diálisis.
- Medicamentos que alteran secreción tubular de
potasio
D. CONTROL DE FOSFATOS
- Mediante control de hidratación y diuresis.
- Quielantes intestinales de fosfatos
- Hidróxido de alumino 50 - 150 mg/kg/d cada
6h por 2 días.
- Sevelamer 20 - 40mg /kg/dosis cada 8h
- Furosemida / diálisis
GRACIAS!

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Sindrome de lisis tumoral.pptx

  • 1. SÍNDROME DE LISIS TUMORAL CUE Alexander Von Humboldt Seminario de Pediatria PRESENTADO POR: Angulo Jose Erazo Stevens Escobar Laura Rodriguez Santiago 2022
  • 2. INTRO/DEFINICIÓN 01 HISTORIA 02 FACTORES RIESGO 04 CLINICA Y DX 05 TABLA DE CONTENIDOS FISIOPATOLOGÍA/ CLASIFICACIÓN 03 TTOS Y ACTUALIZACIÓN 06 WWW.SLIDESGO.COM DISEASE 2022
  • 3. DEFINICION Lisis de células malignas, debida a apoptosis o por la acción de la quimioterapia, se presenta la liberación rápida de elementos intracelulares en cantidades que superan la capacidad de excreción renal, causando alteraciones metabólicas y disfunción orgánica. Hiperuricemia,Hiperpotasemia,Hiperfosfatemia, acompañadas o no de hipocalcemia e insuficiencia renal aguda 2022 01
  • 8.
  • 10. TIPOS DE SÍNDROME DE LISIS TUMORAL
  • 12. PRIMORDIAL EL TIPO DE CA https://slacip.org/manual-slacip/descargas/SECCION-13/13.2- Lisis%20Tumoral-Final.pdf
  • 14.
  • 15. FACTORES DE RIESGO CANCER PRESENTACIÓN CLÍNICA MEDIDAS DE SOPORTE LABORATORIOS Tipo de CA Características del tumor Potencial de lisis celular Potasio exogeno Fosfato exogeno Nefropatias DH Orina Acida Hipotensión Exposición nefrotoxinas LDH Leucos Acido urico y calcemia Creatinina TFG Cristales de ácido úrico Factores que aumentan riesgo evolución
  • 17. Sintomatología depende de la gravedad del trastorno hidroelectrolítico HIPERKALEMIA CARDIACA: arritmias, FA, asistolia, TV, paro NEUROMUSCULAR: debilidad parestesias, espasmos, parálisis flácida HIPERFOSFATEMIA PRECIPITACIÓN RENAL: formación de cristales Nitrógeno ureico y Creatinina HIPOCALCEMIA CARDIOVASCULAR: hipotension, cambios ekg NEUROLÓGICO: tetania, alteraciones musculares, laringoespasmos Estado mental? -- confusion - alucinacion - convulsion HIPERURICEMIA RENAL: nauseas, vomito, oliguria, anuria, anorexia Nitrógeno ureico y Creatinina
  • 19. 1. ESTRATIFICAR FACTORES DE RIESGO Según el tipo de tumor y el recuento de leucocitos 2. MONITORIZAR 3. MANEJO INICIAL 1. Hidratación IV agresiva 2. Hipouricemiantes 3. Control del K+ 4. Control de fosfatos
  • 20. 1. ESTRATIFICAR FACTORES DE RIESGO PARA SLT Pruebas de Laboratorio: - Hemograma + recuento leucocitario - Análisis de orina - Electrolitos - Gases venosos - Calcio, Fosforo, Magnesio - Ácido úrico - BUN - Creatinina - Deshidrogenasa láctica - Pruebas hepáticas - ECG Imágenes - TAC / Ecografía
  • 21. 2. MONITORIZAR DIURESIS SIGNOS VITALES MARCADORES SÉRICOS Cada 4 - 6 horas si hay alto riesgo de SLT
  • 22. 3. MANEJO INICIAL A.HIDRATACIÓN INTRAVENOSA AGRESIVA - ↑ Velocidad de filtrado glomerular. - Iniciar: 24h antes de la quimioterapia; Mantener: 48h Post quimioterapia. Administrar: - 2 - 3 L/m2/d. - 200 ml/kg/d (Si <10kg) Gasto urinario objetivo: - ≥100ml/m2/h - 4 - 6 ml/kg/h (Si <10kg) Se puede adicionar Bicarbonato 40 - 60 mEq / L
  • 23. 3. MANEJO INICIAL B. HIPOURICEMIANTES Alopurinol - Inhibidor de la xantina oxidasa - 12 - 24h antes de la quimioterapia - Se reserva a pacientes con riesgo bajo de SLT Rasburicasa - Degrada el ácido úrico a alantoína - Acción mas rápida (4 horas) - Se reserva a pacientes con niveles muy altos de ácido úrico por su alto costo.
  • 24.
  • 25. 3. MANEJO INICIAL C. CONTROL DEL K+ - Minimizar o suspender los aportes de potasio en los líquidos. - Pacientes asintomáticos: Resinas - Pacientes sintomáticos: - Infusión de insulina + glucosa - Gluconato de calcio - Bicarbonato de sodio - Nebulizaciones de salbutamol - Diálisis. - Medicamentos que alteran secreción tubular de potasio D. CONTROL DE FOSFATOS - Mediante control de hidratación y diuresis. - Quielantes intestinales de fosfatos - Hidróxido de alumino 50 - 150 mg/kg/d cada 6h por 2 días. - Sevelamer 20 - 40mg /kg/dosis cada 8h - Furosemida / diálisis

Editor's Notes

  1. Arritmias potencialmente mortales E insuficeincia renal aguda