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
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
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
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?
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.
