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Hemorragia digestiva
- 1. Encuentra las videosclases en: http://www.youtube.com/channel/UCgZGxUTlxGuZV3MYDcLWEBg?feature=watch
- 2. HEMORRAGIAHEMORRAGIA DIGESTIVADIGESTIVA HECTOR PAUCAR SOTOMAYOR MDHECTOR PAUCAR SOTOMAYOR MD GASTROENTEROLOGIA FMH UNSAAC
- 3. HEMORRAGIA DIGESTIVA DEFINICION EXTRAVASACION DE SANGRE EN EL TUBO DIGESTIVO MELENA – HEMATEMESIS – HEMATOQUEZIA
- 4. HEMORRAGIA DIGESTIVA EPIDEMIOLOGIA 300,000 internamientos hospitalarios/año (USA) Mayor Frecuencia en varones y personas con edad avanzada
- 5. 1.1. HEMORRAGIA DIGESTIVA AGUDAHEMORRAGIA DIGESTIVA AGUDA HEMORRAGIA DIGESTIVA ALTA (HDA) HEMORRAGIA DIGESTIVA BAJA (HDB) HEMORRAGIA DIGESTIVA ORIGEN INDETERMINADO (HDOI) 2.2. HEMORRAGIA DIGESTIVA CRONICAHEMORRAGIA DIGESTIVA CRONICA - ANEMIA FERROPENICA CRONICA - SANGRE OCULTA EN HECES FORMAS CLINICAS
- 6. HEMORRAGIA DIGESTIVA AGUDA MAGNITUD DE HIPOVOLEMIAMAGNITUD DE HIPOVOLEMIA 1. ESTADO HEMODINAMICO: Presion Arterial Frecuencia cardiaca 2. HEMATOCRITO
- 7. HEMORRAGIA DIGESTIVA AGUDA ESTADO HEMODINAMICOESTADO HEMODINAMICO Hemodinamia Perdida de sangre (%) Severidad de la Hemorragia Shock (hipotension en reposo) 20 – 25% Masiva Trastornos posturales (ortostatismo) 10 – 20% Moderada Normal < 10% Leve
- 8. HEMORRAGIA DIGESTIVA AGUDA Hematocrito 0% 10% 20% 30% 40% 50% 60% 70% 80% Antes HD Despues HD 24-72 hs despues HD Plasma Hto
- 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
- 13. TRANSFUSIONES EN HEMORRAGIATRANSFUSIONES EN HEMORRAGIA DIGESTIVADIGESTIVA
- 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 *
- 19. HDA - EPIDEMIOLOGIAHDA - EPIDEMIOLOGIA INCIDENCIAINCIDENCIA: 160 casos x 100,000 hab/año MORTALIDADMORTALIDAD: 8-10% (general) 36% (cirroticos)
- 23. HDA - ETIOLOGIA •ÚÚlcera gástricalcera gástrica •ÚÚlcera duodenallcera duodenal •Gastritis ErosivaGastritis Erosiva •VVarices Esofagicasarices Esofagicas •Mallory-WeissMallory-Weiss Poco FrecuentesPoco Frecuentes • DieulafoyDieulafoy • Ectasias vascularesEctasias vasculares • GastropatiaGastropatia hipertensivahipertensiva • NeoplasiasNeoplasias • EsofagitisEsofagitis RarasRaras •ÚÚlcera Esofagicalcera Esofagica •Duodenitis erosivaDuodenitis erosiva •Fistula aorto/Fistula aorto/ entéricaentérica •HemobiliaHemobilia •Enf. De CrohnEnf. De Crohn •No identificadaNo identificada FrecuentesFrecuentes Longstreth GFLongstreth GF Epidemiology of upper GI bleedingEpidemiology of upper GI bleeding Am J Gastroenterol 90:206 1995Am J Gastroenterol 90:206 1995
- 24. HDA -HDA - ETIOLOGIAETIOLOGIA Luna e cols.Luna e cols. Sobed – Terceira edição – 2000Sobed – Terceira edição – 2000 Estudou 5.345 pacientesEstudou 5.345 pacientes Hospital do Andarai, 75-88 RJHospital do Andarai, 75-88 RJ ÚÚlcera duodenallcera duodenal 31.4 %31.4 % Varices esofágicasVarices esofágicas 24.3 %24.3 % Ulcera gástricaUlcera gástrica 15,0 %15,0 % Lesion aguda de Muc. Gas.Lesion aguda de Muc. Gas. 12.2 %12.2 % Mallory WeissMallory Weiss 3.4 %3.4 % BlastomasBlastomas 3.3 %3.3 % EsofagitisEsofagitis 2.8 %2.8 % Ulcera de anastomosisUlcera de anastomosis 1.3 %1.3 % OtrasOtras 1.7 %1.7 % No determinadasNo determinadas 4.6 %4.6 % PatologiaPatologia Incidencia %Incidencia %
- 25. HOSPITAL NACIONAL “ GUILLERMO ALMENARA ” LIMA - PERU - 1996 SERVICIO DE GASTROENTEROLOGIA Ulcera duodenal 308 36.4 % LAMGD 154 18.2 % Ulcera gástrica 152 17.9 % Varices de esófago 55 6.5 % Neoplasia gástrica 31 3.7 % Duodenitis erosiva 23 2.7 % Mallory Weiss 19 2.2 % Ectasia vascular 15 1.8 % Esofagitis erosiva 6 0.4 % Lesión de Dieulafoy 4 0.4 % Neoplasia de esófago 3 0.4 % Ulcera esofágica 2 0.2 % Neoplasia duodenal 1 0.2 % No especificado 25 2.9 % TOTAL 847 100 %
- 26. CAUSAS DE HDACAUSAS DE HDA ULCERA GASTRICA 39,7% ULCERA DUODENAL 23,3 GASTRITIS HEMORRAGICA 11,5% VARICES E-G 6,4% CANCER GASTRICO 5,1% MALLORY WEISS 3,8% OTROS 18,0% HOSPITAL REGIONAL CUSCO
- 27. TIPOS DE HDA HDA NO VARICEAL HDA VARICEAL
- 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
- 30. DISTRIBUCION ANATOMICA DE LAS VARICES ESOFAGO-GASTRICAS
- 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
- 34. FACTORES PRECIPITANTES Nauseas y Vomitos Tos persistente Maniobra de valsalva Convulsiones Hipo bajo anestesia Trauma abdominal cerrado Masaje toracico Endoscopia
- 38. CANCER GASTRICO
- 43. ECTASIA VASCULAR ANTRAL GASTRICA (ESTOMAGO EN SANDIA)
- 45. ULCERA PEPTICA
- 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
- 52. ULCERA GASTRICAULCERA GASTRICA FORREST IAFORREST IA
- 53. ULCERA GASTRICA FORREST IB
- 54. ULCERA GASTRICAULCERA GASTRICA FORREST IIAFORREST IIA
- 55. ULCERA GASTRICAULCERA GASTRICA FORREST IIBFORREST IIB
- 56. ULCERA GASTRICAULCERA GASTRICA FORREST IICFORREST IIC
- 57. ULCERA DUODENALULCERA DUODENAL FORREST IIIFORREST III
- 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
- 69. PATOGENESIS DE LAS VARICES ESOFAGICAS
- 70. FACTORES QUE INFLUYEN EN EL DESARROLLO DE HEMORRAGIA VARICEAL
- 71. FACTORES QUE INFLUYEN EN LA HEMORRAGIA VARICEAL
- 72. FACTORES QUE INFLUYEN EN LA HEMORRAGIA VARICEAL
- 73. FACTORES QUE INFLUYEN EN LA HEMORRAGIA VARICEAL
- 74. TRATAMIENTO EN LA HDA VARICEAL
- 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
- 80. 1 32 Bandas ElásticasBandas Elásticas
- 81. ENDOLIGADURA DE VARICES ESOFAGICAS (ELVE)
- 83. Clips
- 84. Clips
- 87. TERAPIA DE TAPONAMIENTO: SONDA DE MINNESOTA
- 88. TRANYUGULAR INTRAHEPATIC PORTOSISTEMIC SHUNT (TIPS)
- 90. TIPS
- 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
Notas do Editor
- 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