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Ingestion de causticos
- 1. Encuentra las videosclases en: http://www.youtube.com/channel/UCgZGxUTlxGuZV3MYDcLWEBg?feature=watch
- 2. INGESTA DE CAUSTICOS HECTOR PAUCAR SOTOMAYOR MD CATEDRA DE GASTROENTEROLOGIA FMH - UNSAAC
- 3. Caso clínico: niño de tres años ingiere soda cáustica en polvo
- 4. NIÑOS: 80% de las lesiones por agentes causticos ocurren en niños < 5 años, por descuido de padres o cuidadores ADULTOS: Suicidio o ingestion accidental
- 6. ACIDOS • ACIDO CLORHIDRICO: Acido muriatico, limpia metales, limpiadores de WC, limpiadores de piscinas • ACIDO SULFURICO: Baterias de autos, limpiadores de automoviles • BISULFITO SODICO: Limpiadores de WC • ACIDO OXALICO: Desinfectantes, pulidores de muebles • ACIDO FLUORHIDRICO: Productos antiherrumbre • FORMALDEHIDO: Tabletas desodorantes, Fumigantes, Productos para reparar plastico • ACIDO CARBOLICO (Creso): Antisepticos, preservantes.
- 7. ALCALINOS • HIDROXIDO SODICO O POTASICO (DRANO): Bateria de reloj y calculadoras, detergentes, limpiadores de sumideros, limpiahornos, tabletas de clinitest. • HIPOCLORITO SODICO: Lejias, limpiadores • SALES SODICAS: Detergentes, Productos para lavaplatos electricos, reblandecedores de agua. • AMONIACO: Limpiadores de WC, Limpieza y pulimento de metales, colorantes y tintes para el cabello, productos antiherrumbre, Productos para limpieza de joyas. • PERMANGANATO SODICO: • FOSFORO: Raticidas, insecticidas, Pirotecnia.
- 9. ACIDOS • Necrosis por coagulacion de la albumina, que forma una escara firme y protectora sobre la mucosa que dificulta su penetracion. • Lesiones mas frecuentes en esofago inferior, cardias y zona antropilorica.
- 10. ALCALIS • Necrosis por licuefaccion, con desnaturalizacion de las proteinas, saponificacion de las grasas y trombosis capilar, que pueden provocar perforacion esofagica. • Lesiones mas frecuentes en la boca, faringe y tercio superior del esofago. • Se distingue 4 fases: – Primera fase (1-4 dia): Necrosis con saponificacion, trombosis vascular e intensa reaccion inflamatoria – Segunda fase (3-5 dia): Ulceracion – Tercera fase (5-12 dia): Se inician los procesos reparadores, edema inflamatorio y tejido de granulacion. Es el periodo de maxima debilidad de la pared GI – Cuarta fase (3-4 sem): Cicatrizacion, se inicia progresivamente la estenosis
- 12. CUADRO CLINICO
- 14. Ingestión de cáusticos Preguntas • Existe lesion orofaringea ? • Hubo quemadura de esófago o estómago? • Complicaciones ¿Existe una perforación ? ¿Se producirá una estenosis?
- 15. • ANTECEDENTE DE LA INGESTION • SINTOMAS: LA VARIACION CLINICA ES LA NORMA, QUE PUEDE IR DESDE SINTOMAS ABSOLUTAMENTE INSIGNIFICANTES HASTA ELSHOCK O LA PERFORACION – Disfonia – estridor (lesion de laringe, epiglotis, orofaringe) – Disfagia – odinofagia (lesion de esofago) – Epigastralgia – nauseas – hematemesis (Lesion gastrica) – Taquipnea – disnea – shock con o sin mediastinitis (Perforacion esofagica) – Signos de irritacion peritonea (perforacion gastrica) • EXAMEN FISICO: – Quemadura orofaríngea Wason, J Emerg Med 1985 Crain, Am J dis Child 1984
- 16. Complicación precoz perforación • Signos clinicos: – Esofago: • Enfisema subcutaneo • Dolor retroesternal – Estomago • Signos peritoneales • Rx tórax y abdomen simple • Radiografias contrastadas con contraste hidrosoluble • TAC con contraste hidrosoluble I/C a cirugía
- 19. RADIOGRAFIA DE ESOFAGO CON CONTRASTE HIDROSOLUBLE
- 20. ENDOSCOPIA • Entre 6 y 24 horas • Permite determinar 1. Si hubo lesión mucosa 2. Localización, extensión y severidad
- 22. ENDOSCOPIA
- 25. CRITERIOS ENDOSCOPICOS ESOFAGITIS –GASTRITIS CAUSTICA • Grado 0: Mucosa normal • Grado 1: Hiperemia y edema de la mucosa • Grado 2A: Ulceracion superficial localizada, friabilidad de la mucosa, ampollas. • Grado 2B: Ulceracion circunferencial • Grado 3: Ulceracion profunda y areas extensas de necrosis, con o sin perforación Zargar, Gastrointest Endosc 1991
- 26. RADIOLOGIA
- 33. TRATAMIENTO • 1. MEDIDAS GENERALES: – Prestar especial atencion al aspecto hemodinamico y respiratorio – Intubacion endotraqueal de ser necesario – Infusion de fluidos endovenosos – NPO – SNG (?) – Corticoides y Antibioticos profilacticos (?) – NUTRICION: NPT, Nutricion enteral por yeyunostomia – Contraindicado: El lavado gastrico, induccion del vomito, carbon activado, purgantes.
- 34. DILATACIONES • Desde tercera semana • Bujías de Savary • Balones (TTS) • Método de Tucker • Periodicidad dependerá de cada caso • Corticoides locales?
- 35. Dilatación esofágica 24 h 1 mes 6 meses
- 36. CIRUGIA • CIRUGIA DE EMERGENCIA – Hematemesis severa – Signos radiograficos de perforacion visceral o abdomen agudo – Necrosis caustica extensa • CIRUGIA DE RECONSTRUCCION – Esofagoplastias
- 37. ALGORITMO
Notas del editor
- Figure 7-7. Radiology. Radiologic studies are used during the initial evaluation and resuscitation. Chest radiographs to evaluate for pneumonitis and abdominal films to look for free air signifying hollow viscus perforation should be done. Esophagogram with water-soluble contrast is reserved for patients with suspected perforation.This series of radiographs are from a patient who had four separate barium swallows over a 5-week period following lye ingestion. They demonstrate the progression from acute lye injury to esophageal mucosal repair followed by scarring and stricture formation. In panel A and panel B, taken October 19, proximal esophageal ulceration is seen without evidence of narrowing. In panel C and panel D, taken October 26, there is increased ulcerative changes seen best in the midesophagus. There is some evidence of early narrowing. In panel E and panel F, taken November 6, midesophageal stricture with proximal dilation is also seen. Note in panel G, taken November 17, the long middle to distal esophageal stricture diagnostic for lye stricture. To date no good evidence shows that steroids or antibiotics alter the long-term outcome from lye ingestion except antibiotics in cases of infection. Supportive care and watchful anticipation of possible complication remain the most important aspects of care. Early careful bougienage may be necessary to maintain patency of the esophageal lumen and to prevent future esophagectomy.
- Figure 7-7. Radiology. Radiologic studies are used during the initial evaluation and resuscitation. Chest radiographs to evaluate for pneumonitis and abdominal films to look for free air signifying hollow viscus perforation should be done. Esophagogram with water-soluble contrast is reserved for patients with suspected perforation.This series of radiographs are from a patient who had four separate barium swallows over a 5-week period following lye ingestion. They demonstrate the progression from acute lye injury to esophageal mucosal repair followed by scarring and stricture formation. In panel A and panel B, taken October 19, proximal esophageal ulceration is seen without evidence of narrowing. In panel C and panel D, taken October 26, there is increased ulcerative changes seen best in the midesophagus. There is some evidence of early narrowing. In panel E and panel F, taken November 6, midesophageal stricture with proximal dilation is also seen. Note in panel G, taken November 17, the long middle to distal esophageal stricture diagnostic for lye stricture. To date no good evidence shows that steroids or antibiotics alter the long-term outcome from lye ingestion except antibiotics in cases of infection. Supportive care and watchful anticipation of possible complication remain the most important aspects of care. Early careful bougienage may be necessary to maintain patency of the esophageal lumen and to prevent future esophagectomy.
- Figure 7-69. Endoscopic photograph of acute caustic injury to the esophagus and stomach. A, The esophageal mucosa has a desquamated green appearance with islands of some intact mucosa remaining. B, The stomach has a dark green necrotic appearance without any recognizable mucosa. See also Color Plate. (Courtesy of A. Patrick.)
- Figure 7-69. Endoscopic photograph of acute caustic injury to the esophagus and stomach. A, The esophageal mucosa has a desquamated green appearance with islands of some intact mucosa remaining. B, The stomach has a dark green necrotic appearance without any recognizable mucosa. See also Color Plate. (Courtesy of A. Patrick.)
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.
- Figure 7-70. Radiologic findings in caustic injury to the esophagus. A and B, Acute phase of injury with esophageal ulceration. C and D, Increased ulceration, particularly in midesophagus. E and F, Midesophageal stricture formation with proximal dilation. G, Chronic esophageal stricture formation.