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XXIII CURSO DE ACTUALIZACIÓN DE PATOLOGÍA DIGESTIVA. HEMORRAGIA DIGESTIVA BAJA, HIPERTENSIÓN PORTAL, INTERVENCIÓN QUIRÚRGICA PREVIA. Delgado Plasencia L.J.; Rahy Martín A.; Sánchez-Lauro Martínez M.; Arteaga Glez. I.; Bravo Gutiérrez A.
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XXIII CURSO DE ACTUALIZACIÓN DE PATOLOGÍA DIGESTIVA HEMORRAGIA DIGESTIVA BAJA, HIPERTENSIÓN PORTAL, INTERVENCIÓN QUIRÚRGICA PREVIA Delgado Plasencia L.J.; Rahy Martín A.; Sánchez-Lauro Martínez M.; Arteaga Glez. I.; Bravo Gutiérrez A. S. Cirugía General y Digestiva, H.U.C.
CASO CLINICO • 57 años • Motivo Ingreso: • HD (melenas + rectorragias) • Deterioro nivel conciencia
CASO CLINICO • AP: • Etilismo importante • Cirrosis hepática OH y VHB (Child-Pugh B) • Descompensación ascitico-edematosa • Encefalopatia hepática • Pancreatitis crónica (26 años de evolución) • DMID (16 años de evolución)
CASO CLINICO • Nefropatía diabética; IRC (Cret: 3,7-4,3 mg/dl) • Quirúrgicos: • Puestow • Colecistectomia + coledocoduodenostomia • Reparación eventración * HDA: ulcus bulbar (1995) * HDB: hemorroides interna (1998)
CASO CLINICO: • Acude por HD (rectorragias) + deterioro estado general dos días después de la diálisis. • Encefalopatía hepática grado III • Pruebas complementarias: • Analítica: Hb: 6,4 gr/dl; Hto: 19%. Plaq: 125.000/mm3 • Esofagogastroscopia: varices esofágicas pequeño tamaño y gastropatia hipertensiva H.D.A. Sin repercusión hemodinámica pero con necesidad de transfusión (5 concentrados de Hematies)
CASO CLINICO: Ingreso en UCSI (27/10/03) • Rectorragias + inestabilización hemodinámica (Hto: 22%; Hb: 7,7 gr/dl) • Encefalopatia hepática grado IV. • Transfusión 3 concentrado Hematíes; estabilización hemodinámica • Esofagogastroscopia: • Varices grado I • Gastropatía hipertensiva • Arteriografía: • malformación: conglomerado venoso pericecal que drena hacia la pélvis • No candidato a TIPS
CASO CLINICO Arteriografía:
CASO CLINICO Ingreso en UVI (28/10/03) • 29/10/03: • Melenas y rectorragias Hb: 5 gr/dl; Hto: 27% • Transfusión • Preparación colonoscopia Normal • Hemorragia masiva en la noche del 29 al 30: • 10 concentrados de Hematies • 16 unidades de Plasma • 3 unidades de plaquetas
CASO CLINICO: Opciones terapéuticas • No endoscópicas: no se objetivó el punto de sangrado • Arteriografía: • No TIPS: riesgo inaceptable de encefalopatía hepática • No embolización: • No se objetiva el punto de sangrado • Imposibilidad de embolización circulación venosa aberrante • Cirugía: • Ligadura del plexo varicoso pericecal • Hemicolectomía derecha • Transplante hepático
CASO CLINICO: Cirugía Laparotomía exploradora (30/10/03) • Gran Sd. Adherencial • Varices importantes a nivel de la pared y entre esta y asas de Intestino delgado adheridas • Varices a nivel del mesenterio del yeyuno
H.D.B. Mortalidad del 10-20% Factores predisponentes: • Edad > 60 años • Fallo multiorgánico • Necesidades de transfusión mayores de 5 unidades • Necesidad de cirugía • Situaciones de stress reciente: cirugía, trauma, sepsis
H.D.B. • 1,5 % de las urgencias quirúrgicas • En el 80% ceden espontáneamente • No hay protocolos de actuación
H.D.B. Tres aspectos fundamentales en el tratamiento de la HDB • Determinar la severidad de la hemorragia • Establecer la etiología y localización del sangrado • Tratamiento específico
H.D.B. Etiología y Localización
H.D.B. Tratamiento especifico • Localización conocida: Resección segmentaria • Localización desconocida: • No Colectomía segmentaria: • Resangrado 75% • Morbilidad 83% • Mortalidad 60% • Colectomía subtotal • Resangrado 3% • Morbilidad 32% • Mortalidad 19%
H.D.B. y CIRROSIS HEPATICA ¿Cuáles son las causas de HD en el paciente cirrótico? • Rotura de varices esofágicas y gástricas • Esofagitis por reflujo • LAMG • Ulcera péptica • Disminución de los factores de coagulación
H.D.B. y CIRROSIS HEPATICA Bleeding intestinal varices associated with portal hypertension and previous abdominal surgery.Patients with portal hypertension may develop portasystemic communication in adhesions formed after earlier surgery. This condition causes localized mesenteric and intestinal varices which may lead to significant gastrointestinal hemorrhage. Two patients with this disease spectrum are discussed. The recommended treatment was resection of the involved intestine and formation of a portacaval shunt to eliminate recurrence of the varices and subsequent hemorrhage. Fee. Am Surg. 1977 Nov;43(11):760-2 Scintigraphic demonstration of gastrointestinal bleeding due to mesenteric varices. Mesenteric varices can appear as massive, acute lower gastrointestinal bleeding. The small bowel or colon may be involved, varices usually developing at sites of previous surgery or inflammation in patients with portal hypertension. Hansen; Clin Nucl Med. 1990 Jul;15(7):488-90.
H.D.B. y CIRROSIS HEPATICA Idiopathic mesenteric varices causing lower gastrointestinal bleeding.……. Mesenteric varices are a rare cause of lower gastrointestinal bleeding, almost always associated with portal hypertension. Schilling Eur J Gastroenterol Hepatol. 1996 Feb;8(2):177-9. Characterization of the syndrome of small and large intestinal variceal bleeding. Massive bleeding from jejunal varices in a young alcoholic with cirrhosis and portal hypertension ceased following a portocaval shunt. Although rare, bleeding from small or large bowel varices has a high mortality. In 62 cases, small or large bowel varices are almost always associated with a predisposing condition including previous abdominal surgery and portal hypertension from cirrhosis or other causes. Hematochezia without hematemesis and nonbleeding esophageal varices generally occur. Angiography is the best diagnostic test.Cappell Dig Dis Sci. 1987 Apr;32(4):422-7
H.D.B. y CIRROSIS HEPATICA Gastrointestinal hemorrhage from adhesion-related mesenteric varices.As a result of this retrospective analysis of hemorrhage from a porta-systemic venous shunt occurring within the small intestine, we believe that the early diagnosis of the syndrome is strongly suggested by the presence of varices in unusual locations demonstrated by the venous phase of mesenteric arteriography. In all patients portal hypertension was present, and in all the affected bowel was adherent to postoperative adhesions on old suture lines. The syndrome was treated variously with lysis of adhesions, bowel resection, or portal-systemic shunt. Those patients with excellent hepatic reserve survived and had no further gastrointestinal bleeding. Moncure Ann Surg. 1976 Jan;183(1):24-9 Mesenteric varices: a source of mesosystemic shunts and gastrointestinal hemorrhage.The presence of mesenteric varices was demonstrated angiographically in 7 patients with portal hypertension. In 4 of these cases the mesenteric varices were the source of lower gastrointestinal bleeding which was successfully controlled by intra-arterial infusion of vasopressin. The radiological diagnosis and management of mesenteric varices is discussed and the pertinent literature is briefly reviewed. Federle Gastrointest Radiol. 1979 Nov 15;4(4):331-7
H.D.B. y CIRROSIS HEPATICA Jejunal varices as a cause of massive gastrointestinal bleeding.Jejunal varices are not a common manifestation of portal hypertension. This report describes a 46-yr-old man with recurrent massive gastrointestinal bleeding from jejunal varices arising in an area of adhesions between the intestine and the omentum. The bleeding site was identified by exploratory laparotomy. Medical therapy, including vasopressin infusion via the superior mesenteric artery, was of limited success for controlling acute variceal bleeding. However, jejunal resection and anastomosis resulted in complete resolution of the bleeding, and the patient has experienced no recurrent bleeding over a 3-yr follow-up period. A review of the literature shows that this syndrome is characterized by portal hypertension, generally due to liver cirrhosis; frequently, there is a history of abdominal surgery, and the syndrome presents with hematochezia but without hematemesis. Accurate preoperative diagnosis is often difficult. We propose that bleeding from jejunal varices, though uncommon, should be considered under such clinical conditions. Yuki Am J Gastroenterol. 1992 Apr;87(4):514-7