9. HEMORRAGIA DIGESTIVA AGUDAHEMORRAGIA DIGESTIVA AGUDA
CLASIFICACION CLINICACLASIFICACION CLINICA
HEMORRAGIA DIGESTIVA LEVEHEMORRAGIA DIGESTIVA LEVE
PA SISTOLICA > 100 mm/Hg
FC < 100 LATIDOS POR MINUTO
ORTOSTATISMO NEGATIVO
PIEL CON COLORACION Y TEMPERATURA NORMAL
10. HEMORRAGIA DIGESTIVA AGUDAHEMORRAGIA DIGESTIVA AGUDA
CLASIFICACION CLINICACLASIFICACION CLINICA
HEMORRAGIA DIGESTIVA SEVERAHEMORRAGIA DIGESTIVA SEVERA
DOS O MAS DE LOS SIGUIENTES SIGNOSDOS O MAS DE LOS SIGUIENTES SIGNOS
- PA SISTOLICA < 100 mm/Hg
- FC > 100 LATIDOS POR MINUTO
- ORTOSTATISMO POSITIVO
- HIPOPERFUSION PERIFERICA (SHOCK)
11. MANEJO INICIAL DEL PACIENTE CON
HEMORRAGIA DIGESTIVA AGUDA
Estabilizacion del paciente:
Estabilizacion respiratoria (considerar intubacion
endotraqueal si hay alteracion respiratoria o
hematemesis masiva)
Acceso EV
Reposicion de volumen intravascular
Soluciones cristaloides
Transfusiones (Paquete globular, plasma fresco
congelado, plaquetas)
12. TRANSFUSION SANGUINEA
Importancia de la historia
clinica y examen físico
Historia prévia de anemia
Enfermedad Coronaria
Hemograma y
hematócrito
Hallazgos de la
Endoscopia
14. MANEJO INICIAL DEL PACIENTE CON
HEMORRAGIA DIGESTIVA AGUDA
Historia clinica y examen fisico
Edad
Hemorragia previa
Enfermedades previas (Gastrointestinales, hepaticas)
Cirugia previa
Uso de AINEs
Vomitos persistentes
Perdida de peso
Dolor abdominal
Manifestaciones cutaneas o indicios de enfermedad
hepatica
15. MANEJO INICIAL DEL PACIENTE CON
HEMORRAGIA DIGESTIVA AGUDA
Evaluacion de laboratorio
Hemograma, Hb, Hto, Plaquetas, Gs y Rh
Estudios de coagulacion (TC,TS, TP,TPTA)
Bioquimica sanguinea
Estudios Diagnosticos:
Endoscopia digestiva alta
Estudios radiograficos con bario
Estudios diagnosticos por imágenes con radionuclidos
Angiografia
16. MANEJO INICIAL DEL PACIENTE CON
HEMORRAGIA DIGESTIVA AGUDA
Otros examenes auxiliares (condicionales)
Radiografia de abdomen simple (sospecha de perforacion)
Electrocardiograma
Localizacion del sitio de sangrado
HDA VS HDB
Historia clinica adecuada
Lavado nasogastrico
Indice urea/creatinina incrementado
Interconsultas
Gastroenterologia (Para endoscopia)
Cirugia
18. HDA : DEFINICION
EXTRAVASACION DE SANGRE EN EL TUBO
DIGESTIVO EN LA PORCION COMPRENDIDA
ENTRE EL ESOFAGO Y EL ANGULO DE TREIZT
MELENA – HEMATEMESIS
HEMATOQUEZIA *
28. HDA NO VARICEAL
Implica perdida sanguinea proveniente de
arteria o arteriolas
La ulcera peptica es la principal causa de
HDA no variceal
Otras causas : Gastritis erosiva, ulcera de
stress, Lesion de Mallory Weiss.
29. Alta mortalidad (20-50%) dependiendo
del estado clinico y de la severidad de
la hemorragia.
Sangrado asociado a Hipertension
portal y Cirrosis
HDA VARICEAL
32. ESOFAGITISESOFAGITIS
Aproximadamente 3% de HDAsAproximadamente 3% de HDAs
Sangrado leveSangrado leve
Tratamiento con IBP y medidasTratamiento con IBP y medidas
anti-reflujoanti-reflujo
Pocas opçiones endoscópicas dePocas opçiones endoscópicas de
tratamientotratamiento
46. ULCERA PEPTICA
FACTORES PREDISPONENTES PARAFACTORES PREDISPONENTES PARA
LA HEMORRAGIALA HEMORRAGIA
1. Acido gastrico
2. Helicobacter pylori
3. Etanol
4. AINEs
5. Otros agentes farmacologicos: Corticoides,
anticoagulantes, alendronato
47. Criterios Clínicos de Alto RiesgoCriterios Clínicos de Alto Riesgo
Edad > 60 años
Enfermedades graves
asociadas
Hospitalizaciones
frecuentes
Hematemesis o
enterorragia de inicio
Melena persistente
Hipotension ortostática
Presion sistólica < 100
mm HG
Pulso > 100 x min
Resangrado
Transfusiones - > 4U en
las primeras 24h
Resangrado
48. FACTORES PRONOSTICOS EN LA
HDA POR ULCERA PEPTICA
CRITERIOS ENDOSCOPICOS DE MALCRITERIOS ENDOSCOPICOS DE MAL
PRONOSTICOPRONOSTICO
ULCERA DE DIAMETRO MAYOR A 2 CM.
LOCALIZACION:
CARA POSTERIOR DE BULBO DUODENAL
CURVATURA MENOR DEL ESTOMAGO
PROFUNDIDAD : > PROFUNDIDAD > SANGRADO
APARIENCIA DEL LECHO ULCEROSO
49. FACTORES PRONOSTICOS EN LA HDA
POR ULCERA PEPTICA
CLASIFICACION DE FORREST
FORREST I (sangrado activo)
Ia -------- Sangrado en chorro
Ib ---------> Sangrado en napa
FORREST II (Sangrado reciente)
IIa ------ Vaso visible
IIb -------> Coagulo adherido
IIc ------ Manchas planas, rojas marrones en
nicho ulceroso
FORREST III ( No hay sangrado activo)
50. Clasificación Descripción Prevalencia Resangrado
Forrest IForrest I
SangradoSangrado
activoactivo
IaIa Chorro arterialChorro arterial 10%10% 90%90%
IbIb
Sangrado enSangrado en
napanapa
5%5% <20%<20%
Forrest IIForrest II
SangradoSangrado
recientereciente
IIaIIa Vaso visibleVaso visible 25%25% 50%50%
IIbIIb
CoáguloCoágulo
adheridoadherido
10%10% 25%25%
IIcIIc Lecho “sucio”Lecho “sucio” 15%15% <10%<10%
Forrest IIIForrest III
Lecho de úlceraLecho de úlcera
“limpio”“limpio”
35%35% <5%<5%
51. Estigmas de sangrado y riesgo de
resangrado
0
10
20
30
40
50
60
70
80
90
chorro V. visible Coag. Adh. Resuma Mancha sucia Limpio
Resangrado
58. HDA NO VARICEAL
TRATAMIENTO
TRATAMIENTO MEDICO
• NPO
• MONITORIZACION APROPIADA
• REPOSICION DE VOLUMEN:
• CRISTALOIDES
• TRANSFUSION COMPONENTES SANGUINEOS
• Paquete globular
• Plasma Fresco Congelado
• COLOCACION DE SNG
• SUPRESION DE LA SECRECION ACIDA
59. HDA NO VARICEAL
TRATAMIENTO MEDICO
Omeprazol (80 mg EV en bolo,
seguido de infusion de 8 mg/hr por
72 horas, reduce el riesgo de
resangrado en pacientes con ulcera
sangrante y con factores de alto
riesgo.
60. HDA NO VARICEAL
TRATAMIENTO ENDOSCOPICO
METODOS TERMICOS
. Rayo laser (Nd:YAG)
. Electrocoagulacion bipolar
. Probeta caliente
. Argon plasma
METODOS POR INYECCION DE SUSTANCIAS QUIMICAS
. Adrenalina (1/10,000)
. Etanol absoluto
. Agentes esclerosantes
AGENTES TOPICOS
. Adhesivo de fibrina
AGENTES MECANICOS
. Endoclips
. Endoloop
. Ligadura con banda
61. TRATAMIENTO DE HDA PORTRATAMIENTO DE HDA POR
ÚLCERA GÁSTRICA O DUODENALÚLCERA GÁSTRICA O DUODENAL
Soluciones usadas em la terapia porSoluciones usadas em la terapia por
injeccion en úlceras hemorrágicasinjeccion en úlceras hemorrágicas
Solucion Mecanismo de accionSolucion Mecanismo de accion VolumenVolumen
Alcohol absolutoAlcohol absoluto Deshidratacion y fijacionDeshidratacion y fijacion 1 a 4 ml1 a 4 ml
Etanolamina ( 1 a 5%)Etanolamina ( 1 a 5%) Trombosis + lesion de la íntimaTrombosis + lesion de la íntima 5 a 20 ml5 a 20 ml
Polidocanol 1 %Polidocanol 1 % idemidem 5 ml5 ml
Adrenalina 1: 10000Adrenalina 1: 10000 Vasoconstriccion u agregacion plaquetáriaVasoconstriccion u agregacion plaquetária 5 a 50 ml5 a 50 ml
62. HDA NO VARICEAL
TRATAMIENTOTRATAMIENTO QUIRURGICO
HEMORRAGIA NO CONTROBLE (EX-SANGUINANTE)
FRACASO AL TRATAMIENTO ENDOSCOPICO:
PRIMARIO: VISION, POSICION, CUANTIA, TIPO DE LESION.
RECURRENCIA LUEGO DE 2da TERAPIA ENDOSCOPICA
NECESIDAD DE MAS DE 5 UNIDADES DE SANGRE (?)
63. HEMORRAGIA DIGESTIVA NO VARICEAL
Estimar volumen de la perdida sanguinea
Hb,Hto, Hem, Pruebas de coagulacion, GS y rH
Via central, PVC,
SNG (lavado con agua)
Sonda Foley (volumen urinario)
MONITOREO DE PA, PULSO, FR
Sangrado inactivo
Hemodinamia estable
No enfermedad concomitante
Perdida < 500 cc
Sangrado activo
Inestabilidad hemodinamica
Enfermedad concomitante
Perdida 1000-1500 cc
Hemorragia masiva
Inestabilidad hemodinamica
Perdida > 2000cc
Hospitalizar en Medicina
Endoscopia alta
Tratamiento oral
UCI – UHD
Estabilizacion hemodinamica
SNG (lavado con agua)
Evaluacion por Cirugia
Endoscopia urgente
Algoritmo 2
Si no es posible
Tratamiento quirurgico
64. HEMORRAGIA DIGESTIVA NO VARICEAL
ENDOSCOPIA ALTA URGENTE
(ALGORITMO 2)
Lesion controlable con
coagulacion o
escleroterapia
Lesion no tributaria de
coagulacion o escleroterapia
Endoscopia
insuficiente
Malformacion AV
Sindrome de Mallory
Weiss
Ulcera peptica (FIa, Ib,IIa)
Terapia endoscopica
Continua sangrado o
Recurrencia
Gastritis
Esofagitis
Cancer gastrico
Cesa sangrado
Continua tratamiento
EV u oral
Monitorizar FV
Continuar Bloq. H2 o IBP
Cirugia
Re-evaluacion
Tratamiento de acuerdo a
evidencia de sangrado
76. HDA VARICEAL
TRATAMIENTO FARMACOLOGICO
VASOCONSTRICTORES
Octreotide: 50-100 ugr en bolo EV-SC, luego infusion a 25 - 50
ugr/hora EV.
Vasopresina: 20 U en bolo (15 min), luego 0.2 – 0.4 U /min. EV.
Terlipresina: 1-2 mg EV c/4-6 hs
VASODILATADORES:
Mononitrato de isosorbide: 7.5 mg c/30 min x 6 hs.
OTROS AGENTES:
Metoclopramida, Domperidona (?)
77. HDA VARICEAL
TRATAMIENTO ENDOSCOPICO
Escleroterapia de varices esofagicas (EVE)
Endoligadura de varices esofagicas (ELVE)
Inyecccion de cianoacrilato en varices de fondo gastrico
Clips endoscopicos
Endoloop endoscopico
TAPONAMIENTO
Sonda de Sengstaken Blackemore
Sonda de Minnesota
TIPS
TRATAMIENTO QUIRURGICO
92. HEMORRAGIA DIGESTIVA VARICEAL
Estimar volumen de la perdida sanguinea
Hb,Hto, Hem, Pruebas de coagulacion, GS y Rh
Via central, PVC,
SNG (lavado con agua)
Sonda Foley (volumen urinario)
MONITOREO DE PA - PULSO – FR
UCI - UHD
Gastropatia hipertensiva portal
OCTREOTIDE
Angiografia terapeutica
Cirugia de urgencia
Endoscopia alta urgente
Endoscopia
deficiente
Varices esofagicas
Escleroterapia o
endoligadura
Balon de STB durante 24 hs
con o sin
Vasopresina
Octreotide
No cesa: TIPS – CLIPS - CIRUGIA Cesa: EVE – ELVE - PROPANOLOL
Notes de l'éditeur
Figure 11-25. Anatomic distribution of gastroesophageal varices (GOVs). GOVs, which are part of the anatomic constellation of portal hypertensive gastropathy, are poorly understood and defined. Sarin and coworkers [35] in New Delhi have classified GOVs. Those GOVs, which are continuous with esophageal varices, may involve the lesser (GOV1) or the greater curvature (GOV2) of the stomach. Type 1 isolated gastric varices (IGV1), which are not continuous with esophageal varices, are usually found in the fundus of the stomach. Type 2 IVGs (IGV2) may be found anywhere in the stomach and are prone to bleed; type 2 isolated ectopic varices tend not to bleed. Sarin and and coworkers [35] comment about the prevalence and the distribution of these two types of varices and their clinical behavior. (Adapted from Sarin et al. [35].) References: [35]. Sarin SK, Lahoti D, Saxena SP, Prevalence, classification and natural history of gastric varices. a long-term follow-up study in 568 portal hypertension patients. Hepatology 1992 16 1343-1349
Figure 11-1. Precipitating factors for Mallory-Weiss tears. These were first described in 1929 by Mallory and Weiss in alcoholic patients with retching and vomiting followed by often massive, rarely fatal upper gastrointestinal bleeding. These tears are short, linear mucosal lacerations occurring at the gastroesophageal junction, often in association with hiatal hernia, usually following an initial traumatic episode of retching and nonbloody emesis. If a tear involves a vessel, bleeding may be seen and can be severe. Precipitating factors resulting in Mallory-Weiss tears involve processes that rapidly increase intra-abdominal pressure such as retching [1], [2], [3]. References: [1]. Weaver DH, Maxwell JG, Castleton KB, Mallory-Weiss syndrome. Am J Surg 1969 18 887 [2]. Watts HD, Admirand WH, Mallory-Weiss syndrome: a reprisal. JAMA 1974 230 1674 [3]. Michel L, Serrano A, Melt RA, Mallory-Weiss syndrome: evolution of diagnostic and therapeutic patterns over two decades. Ann Surg 1980 192 716
Figure 9-8. Hemorrhagic gastritis. Gastritis is a histologic term that does not necessarily correlate with the endoscopic appearance. Gastritis or more precisely, gastropathy, usually occurs in the setting of stress, alcohol abuse, or nonsteroidal anti-inflammatory drug use. This figure is an extreme example of hemorrhagic gastritis. There are several areas of confluent subepithelial hemorrhage (with an appearance of blood under plastic wrap) separated by areas of eroded mucosa.
Figure 9-20. Cardia carcinoma. The gastric cardia is that portion of the stomach immediately adjoining the esophagus. Because of the proximity to the esophagus, carcinoma of the gastric cardia can result in dysphagia. This carcinoma is seen on retroflexion view and has a friable, necrotic appearance. Surgical resection of such a tumor is challenging because it may require an esophagectomy in addition to a partial gastrectomy.
Figure 9-12. Dieulafoy's lesion. Dieulafoy's lesion is a rare cause of massive and recurrent upper gastrointestinal hemorrhage. The lesion is an extramural caliber artery present in the submucosa. Bleeding probably results from pressure exerted by such a blood vessel on the overlying mucosa so that it is ultimately exposed to the lumen. Dieulafoy's lesion is most common in the gastric cardia, 6 cm from the gastroesophageal junction. Mortality is high because the bleeding site is often difficult to identify. A, Rarely Dieulafoy's lesion may have the appearance of a visible blood vessel in the absence of an ulcer crater. B, When exposed to the lumen, the vessel's wall may actually break down and lead to dramatic bleeding [12]. References: [12]. Eidus L, Rasuli P, Manion D, Heringer R, Caliber-persistent artery of the stomach. Gastroenterology 1990 99 1507-1510
Figure 9-12. Dieulafoy's lesion. Dieulafoy's lesion is a rare cause of massive and recurrent upper gastrointestinal hemorrhage. The lesion is an extramural caliber artery present in the submucosa. Bleeding probably results from pressure exerted by such a blood vessel on the overlying mucosa so that it is ultimately exposed to the lumen. Dieulafoy's lesion is most common in the gastric cardia, 6 cm from the gastroesophageal junction. Mortality is high because the bleeding site is often difficult to identify. A, Rarely Dieulafoy's lesion may have the appearance of a visible blood vessel in the absence of an ulcer crater. B, When exposed to the lumen, the vessel's wall may actually break down and lead to dramatic bleeding [12]. References: [12]. Eidus L, Rasuli P, Manion D, Heringer R, Caliber-persistent artery of the stomach. Gastroenterology 1990 99 1507-1510
Figure 9-10. Watermelon stomach [11]. This lesion results from multiple antral vascular ectasias formed in a pattern of linear streaks radiating from the pylorus. Histologically, it consists of multiple dilated venules with focal thrombosis and fibromuscular hyperplasia. The cause of watermelon stomach is not known but it occurs primarily in older women. It presents with iron-deficient anemia, which is usually manageable with iron supplementation. In extreme cases, endoscopic thermal therapy or surgical antrectomy may be necessary. References: [11]. Jabbari J, Cherry R, Lough J, et al. Gastric antral vascular ectasia: The watermelon stomach. Gastroenterology 1984 87 1165-1170
Figure 11-6. Pathogenesis of esophageal varices. Esophageal (and gastric) varices are enlarged veins that are part of the extensive collateral circulation that can develop in the setting of portal hypertension (A). In normal individuals, almost 100% of portal venous flow (approximately 1 L/min) is recoverable in the hepatic vein, whereas in the patient with cirrhosis up to 87% may be directed into collateral flow. Although varices can develop in many areas, they are most problematic in the esophagus (and proximal stomach), wherein life-threatening hemorrhage may occur. Increased portal venous pressure is most commonly secondary to cirrhosis from a variety of causes, but can be caused by noncirrhotic liver disease or from extrahepatic causes. Systemic vasodilation with decreased vascular resistance and the formation of a hyperdynamic circulation may also play a role in the development of portal hypertension and subsequent varices. It has been estimated that this increased flow is responsible for 40% of the increase, and that resistance to flow is responsible for 60% of the increase in portal pressure in cirrhosis. B, Active hemorrhage from a distal esophageal varix with a sclerotherapy injector at the 7-o'clock position. (A adapted from Waye [8].) References: [8]. Waye JD, Esophageal variceal sclerotherapy. In Techniques in Therapeutic Endoscopy. Edited by Geenen J, Fleischer DE, Waye JD. New York: Gower Medical Publishing; 1992 3.1-3.12
Figure 11-6. Pathogenesis of esophageal varices. Esophageal (and gastric) varices are enlarged veins that are part of the extensive collateral circulation that can develop in the setting of portal hypertension (A). In normal individuals, almost 100% of portal venous flow (approximately 1 L/min) is recoverable in the hepatic vein, whereas in the patient with cirrhosis up to 87% may be directed into collateral flow. Although varices can develop in many areas, they are most problematic in the esophagus (and proximal stomach), wherein life-threatening hemorrhage may occur. Increased portal venous pressure is most commonly secondary to cirrhosis from a variety of causes, but can be caused by noncirrhotic liver disease or from extrahepatic causes. Systemic vasodilation with decreased vascular resistance and the formation of a hyperdynamic circulation may also play a role in the development of portal hypertension and subsequent varices. It has been estimated that this increased flow is responsible for 40% of the increase, and that resistance to flow is responsible for 60% of the increase in portal pressure in cirrhosis. B, Active hemorrhage from a distal esophageal varix with a sclerotherapy injector at the 7-o'clock position. (A adapted from Waye [8].) References: [8]. Waye JD, Esophageal variceal sclerotherapy. In Techniques in Therapeutic Endoscopy. Edited by Geenen J, Fleischer DE, Waye JD. New York: Gower Medical Publishing; 1992 3.1-3.12
Figure 11-7. Factors involved in variceal hemorrhage. The lifetime risk for bleeding from esophageal varices has been estimated at 10% to 67%, with the probable risk being from 30% to 40%. Multiple factors have been proposed to identify varices at higher risk for hemorrhage. A portal pressure of at least 12 mmHg appears to be necessary for the development of varices and for significant hemorrhage. Higher pressures, however, do not correlate with greater bleeding risk. Variceal size appears to have some predictive value, and perhaps wall thickness does as well, particularly in how they contribute to wall tension (t). Wall tension in larger varices will be greater than in smaller varices with the same intravariceal pressure (p). Wall tension also varies inversely with the thickness of the variceal wall (W). A, These relationships are demonstrated in the modification of Laplace's law [9], [10]. BD, `Red color´ signs also appear to portend a greater risk of bleeding; when seen on large varices they are particularly worrisome. They represent `varices on varices´ and probably correspond histologically with dilated intraepithelial venules. Also note the fibrin-platelet plugs (panels C and D) which identify the site of recent hemorrhage and provide useful information to the endoscopist. References: [9]. Polio J, Grosmann RJ, Hemodynamic factors involved in the development and rupture of oesophageal varices: A pathophysiologic approach to treatment. Semin Liver Dis 1986 6 318 [10]. Kaplowitz N, Pathophysiology of portal hypertension. In Liver and Biliary Diseases. Edited by Kaplowitz N. Baltimore: Williams & Wilkins; 1992 499-503
Figure 11-7. Factors involved in variceal hemorrhage. The lifetime risk for bleeding from esophageal varices has been estimated at 10% to 67%, with the probable risk being from 30% to 40%. Multiple factors have been proposed to identify varices at higher risk for hemorrhage. A portal pressure of at least 12 mmHg appears to be necessary for the development of varices and for significant hemorrhage. Higher pressures, however, do not correlate with greater bleeding risk. Variceal size appears to have some predictive value, and perhaps wall thickness does as well, particularly in how they contribute to wall tension (t). Wall tension in larger varices will be greater than in smaller varices with the same intravariceal pressure (p). Wall tension also varies inversely with the thickness of the variceal wall (W). A, These relationships are demonstrated in the modification of Laplace's law [9], [10]. BD, `Red color´ signs also appear to portend a greater risk of bleeding; when seen on large varices they are particularly worrisome. They represent `varices on varices´ and probably correspond histologically with dilated intraepithelial venules. Also note the fibrin-platelet plugs (panels C and D) which identify the site of recent hemorrhage and provide useful information to the endoscopist. References: [9]. Polio J, Grosmann RJ, Hemodynamic factors involved in the development and rupture of oesophageal varices: A pathophysiologic approach to treatment. Semin Liver Dis 1986 6 318 [10]. Kaplowitz N, Pathophysiology of portal hypertension. In Liver and Biliary Diseases. Edited by Kaplowitz N. Baltimore: Williams & Wilkins; 1992 499-503
Figure 11-7. Factors involved in variceal hemorrhage. The lifetime risk for bleeding from esophageal varices has been estimated at 10% to 67%, with the probable risk being from 30% to 40%. Multiple factors have been proposed to identify varices at higher risk for hemorrhage. A portal pressure of at least 12 mmHg appears to be necessary for the development of varices and for significant hemorrhage. Higher pressures, however, do not correlate with greater bleeding risk. Variceal size appears to have some predictive value, and perhaps wall thickness does as well, particularly in how they contribute to wall tension (t). Wall tension in larger varices will be greater than in smaller varices with the same intravariceal pressure (p). Wall tension also varies inversely with the thickness of the variceal wall (W). A, These relationships are demonstrated in the modification of Laplace's law [9], [10]. BD, `Red color´ signs also appear to portend a greater risk of bleeding; when seen on large varices they are particularly worrisome. They represent `varices on varices´ and probably correspond histologically with dilated intraepithelial venules. Also note the fibrin-platelet plugs (panels C and D) which identify the site of recent hemorrhage and provide useful information to the endoscopist. References: [9]. Polio J, Grosmann RJ, Hemodynamic factors involved in the development and rupture of oesophageal varices: A pathophysiologic approach to treatment. Semin Liver Dis 1986 6 318 [10]. Kaplowitz N, Pathophysiology of portal hypertension. In Liver and Biliary Diseases. Edited by Kaplowitz N. Baltimore: Williams & Wilkins; 1992 499-503
Figure 11-7. Factors involved in variceal hemorrhage. The lifetime risk for bleeding from esophageal varices has been estimated at 10% to 67%, with the probable risk being from 30% to 40%. Multiple factors have been proposed to identify varices at higher risk for hemorrhage. A portal pressure of at least 12 mmHg appears to be necessary for the development of varices and for significant hemorrhage. Higher pressures, however, do not correlate with greater bleeding risk. Variceal size appears to have some predictive value, and perhaps wall thickness does as well, particularly in how they contribute to wall tension (t). Wall tension in larger varices will be greater than in smaller varices with the same intravariceal pressure (p). Wall tension also varies inversely with the thickness of the variceal wall (W). A, These relationships are demonstrated in the modification of Laplace's law [9], [10]. BD, `Red color´ signs also appear to portend a greater risk of bleeding; when seen on large varices they are particularly worrisome. They represent `varices on varices´ and probably correspond histologically with dilated intraepithelial venules. Also note the fibrin-platelet plugs (panels C and D) which identify the site of recent hemorrhage and provide useful information to the endoscopist. References: [9]. Polio J, Grosmann RJ, Hemodynamic factors involved in the development and rupture of oesophageal varices: A pathophysiologic approach to treatment. Semin Liver Dis 1986 6 318 [10]. Kaplowitz N, Pathophysiology of portal hypertension. In Liver and Biliary Diseases. Edited by Kaplowitz N. Baltimore: Williams & Wilkins; 1992 499-503
Figure 11-9. Endoscopic sclerotherapy. This technique has been used in previous years as an effective treatment for acute variceal hemorrhage and for prophylaxis for recurrent hemorrhage after the initial bleeding episode has stopped. Both paravariceal and intravariceal injection techniques have been recommended. Regardless of the location of the external puncture, the depth of needle penetration may be difficult to control and may range from intravariceal to submucosal, or into the muscular layer, the latter perhaps predisposing to deeper ulceration (A). The preferred technique is for injections of 1 mL to 2 mL of sclerosant into the varix starting as distally in the esophagus as possible (near or just below the esophageal-gastric junction) and in a circumferential route. Injections are then repeated 2 cm to 5 cm more proximally (B). The total volume of sclerosant should not exceed 20 mL per session, above which rate the incidence of complications may increase. No particular sclerosant has emerged as consistently superior; sodium tetradecyl, ethanolamine oleate, absolute ethanol, and sodium morrhuate are agents available in the United States. (Adapted from Waye [8].) References: [8]. Waye JD, Esophageal variceal sclerotherapy. In Techniques in Therapeutic Endoscopy. Edited by Geenen J, Fleischer DE, Waye JD. New York: Gower Medical Publishing; 1992 3.1-3.12
Figure 11-9. Endoscopic sclerotherapy. This technique has been used in previous years as an effective treatment for acute variceal hemorrhage and for prophylaxis for recurrent hemorrhage after the initial bleeding episode has stopped. Both paravariceal and intravariceal injection techniques have been recommended. Regardless of the location of the external puncture, the depth of needle penetration may be difficult to control and may range from intravariceal to submucosal, or into the muscular layer, the latter perhaps predisposing to deeper ulceration (A). The preferred technique is for injections of 1 mL to 2 mL of sclerosant into the varix starting as distally in the esophagus as possible (near or just below the esophageal-gastric junction) and in a circumferential route. Injections are then repeated 2 cm to 5 cm more proximally (B). The total volume of sclerosant should not exceed 20 mL per session, above which rate the incidence of complications may increase. No particular sclerosant has emerged as consistently superior; sodium tetradecyl, ethanolamine oleate, absolute ethanol, and sodium morrhuate are agents available in the United States. (Adapted from Waye [8].) References: [8]. Waye JD, Esophageal variceal sclerotherapy. In Techniques in Therapeutic Endoscopy. Edited by Geenen J, Fleischer DE, Waye JD. New York: Gower Medical Publishing; 1992 3.1-3.12
Figure 11-12. Endoscopic variceal band ligation. AD, Endoscopic views of variceal band ligation that correspond to the sequence of steps discussed in Figure 11-11.
Figure 11-8. Options in acute variceal hemorrhage. Endoscopic therapy is useful in the management of acute variceal hemorrhage. Other options include medical treatment, first tamponade with a Sengstaken-Blakemore tube or a Minnesota tube (pictured), placement of an intrahepatic shunt (ie, transjugular-intrahepatic portosystemic shunt) placed by vascular interventional radiology, or surgical intervention. Vasoactive drugs such as octreotide, vasopressin, nitroglycerin, and terlipressin are effective in the acute setting in decreasing bleeding by lowering portal pressures. Some gastroenterologists feel that concurrent use of vasoactive drugs during endoscopic treatment of acute bleeding improves visualization and outcome, although this has not been proven. Despite all these options, the 1-year survival rate after initial hemorrhage has changed little over the last 50 years, and remains about 40%.
Figure 11-12. Transjugular intrahepatic portosystemic stent shunts. This diagram demonstrates how the stent connects the hepatic vein or one of its branches to the portal vein or one of its branches [14]. (Adapted from McCormick et al. [14].) References: [14]. McCormick PA, Dick R, Irving JD, et al. Transjugular intrahepatic portosystemic stent-shunt. J Hosp Med 1993 49 28-32
Figure 11-13. Wallstent for transjugular intrahepatic portosystemic stent shunts. A stainless steel mesh stent with a 10-mm diameter is shown. The flexibility of this stent, which is obvious in this photograph, is its greatest virtue. This flexibility permits it to be positioned in sharp curves without significant distortion in shape. (Courtesy of A. Florey, Minneapolis, MN)
Figure 11-14. Plastic cast of Wallstent transjugular intrahepatic portosystemic stent shunts in situ. This patient's liver had been resected before liver transplantation. The hepatic vein was injected with blue plastic and the portal vein with white plastic. The transected right hepatic vein is seen in the upper right. A long, double-length stent extends from the right hepatic vein to the right portal vein. (Courtesy of J.P. Vinel, Toulouse, France)
Figure 11-6. Transjugular intrahepatic portosystemic shunt (TIPS). This hepatic Doppler sonogram in a 55-year-old man with alcoholic cirrhosis and portal hypertension shows the position of a patent TIPS [5]. The procedure was performed because of refractory, debilitating ascites. The shunt shows characteristic echogenicity (solid arrows) and an intense blue signal caused by shunted blood flow. Ascites (open arrow) is present anterior to the liver. After the placement of the shunt, the patient's esophageal varices diminished in size and the ascites began to disappear without further therapy. The patient was awaiting liver transplantation at the time of this ultrasonographic examination. The shunt became occluded 8 months later. (From Sadler and Shapiro [5]; with permission.) References: [5]. Sadler MA, Shapiro RS, Transjugular portosystemic shunt. N Engl J Med 1994 330(3) 182