DIAGNÓSTICO DIFERENCIAL Y MANEJO DE LA ASCITIS · PDF fileVer higado y bazo: si ≥12...

DIAGNÓSTICO DIFERENCIAL Y MANEJO DE LA ASCITIS

MARI CRUZ PÉREZ PANIZOMIR MEDICINA INTERNA

COMPLEJO ASISTENCIAL UNIVERSITÁRIO DE LEÓN11-6-2012

SESIONES BIBLIOGRSESIONES BIBLIOGRÁÁFICAS RESIDENTESFICAS RESIDENTES

Servicio Medicina Interna

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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISCausas

-Obesidad abdominal- distinguir ascitis de grasa: tiempo de evolución-Cirrosis: causa más frecuente de ascitis-Hepatitis alcohólica con o sin cirrosis-Hepatitis viral C: transfusiones antes de 1990, compartir agujas, tatuajes, acunpuntura,emigración A Japón ó sudeste asiático-Hepatitis B: tranfusion antes de 1971, áreas hiperendemicas (África, Sudeste asiático:China, Corea, Indonesi y Filipinas, oriente medio excepto Israel, islas del pacifico sur y oeste, cuenca interior del Amazonas y partes del Caribe: Haití y R.Dominicana), varones homosexuales, UDVP, Dialisis, VIH y contactos.-Historia familiar de enfermedad hepática: Hemocromatosis, Wilson-Esteatohepatitis no alcohólica: antes criptogenética: obesidad, DM, DL: riesgo de “ “ “ según nº de años con IMC>30Kg/m2

-Complicación de una cirrosis compensada: por daño hepático viral o hepático sobre la previa cirrosis, desarrollo de hepatocarcinoma-si no cumple anamnesis ni caracteristicas clinicas ni pruebas complementarias de cirrosis: otras causas: cancer, ICC, TBC, Hemodialisis (ascitis nefrogénica) y pancreatitis.


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CAUSES OF ASCITES

Cirrhosis 81 percentCancer 10 percentHeart failure 3 percentTuberculosis 2 percentDialysis 1 percentPancreatic disease 1 percentOther 2 percent


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Data from: Runyon, BA, Hoefs, JC, Morgan, TR. Ascitic fluid analysis in malignancy‐related ascites. Hepatology 1998;

8:1104.

Causes of malignancy‐related ascites

Cause Frequency among patients with malignancyrelated ascites

Peritoneal carcinomatosis 53 percent

Massive liver metastases causing portal hypertension

13 percent

Peritoneal carcinomatosis plus massive liver metastases

13 percent

Hepatocellular carcinoma plus cirrhosis 13 percent

Chylous ascites due to malignancy, usually lymphoma

7 percent

Budd‐Chiari syndrome due to malignancy occluding the hepatic veins

Rare


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Rare causes of ascites

Miscellaneous Abdominal pregnancy

Crohn's disease

Mastocytosis

Endometriosis

Gaucher's disease

Lymphangioleiomyomatosis

Myxedema

Nephrotic syndrome (in children, adults with nephrotic syndrome and ascites usually have another cause such as cirrhosis)

Operative lymphatic tear or ureteral injury

Ovarian hyperstimulation syndrome

POEMS syndrome

Systemic lupus erythematosus

Ventriculoperitoneal shunt


Hematologic Amyloidosis

Castleman's syndrome

Extramedullary hematopoiesis

Hemophagocytic syndrome

Histiocytosis X

Leukemia

Lymphoma

Multiple myeloma


Infectious

Amebiasis

Ascariasis

Brucellosis

Chlamydia peritonitis

Complications related to HIV infection

Pelvic inflammatory disease

Salmonellosis

Pseudomembranous colitis

Whipple's disease


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CAUSA MÁS FRECUENTE DE ASCITIS: CIRROSIS HEPCIRROSIS HEPÁÁTICA:TICA:

1.COMPLICACIONES POR LA HTPORTAL:-HDA POR VARICES ESOFÁGICAS O POR GASTROPATÍA DE LA HTP-ASCITIS: ES LA COMPLICACIÓN MÁS FRECUENTE-EPH2.COMPLICACIONES POR LA ASCITIS:-PBE-SÍNDROME HEPATORRENAL


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ASCITIS DEBIDA A MÁS DE UNA CAUSA:5% de pacientes aprox.Diagnóstico más confuso: cada causa por separado no es tan severa como para provocar la cuantía ascítica observada

Las más frecuentes que coexisten:

Cirrosis + peritonitis TBC“ + carcinomatosis peritoneal“ + ICC“ + nefropatía diabéticaComplicaciones obesidad: nefropatia diabética + ICC + cirrosis debida a Esteatohepatitis no alcohólica


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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISExploración física

Estigmas de cirrosis: excepción el paciente de pigmentación oscura (no son aparentes ni las arañas vasculares ni el eritema palmar), colaterales abdominales de extensión cefálica, son raras las arañas vasculares por debajo del ombligo.IctericiaPérdida de masa muscularLeuconiquia: uñas de Muehrcke, TerryHipertrofia parotídea bilateral (por alcohol y no por la cirrosis en si)Hepatoesplenomegalias palpables (puede)Palpación hepática: blando, grande y firme más en hepatitis enólica que en hepatocarcinomaPrincipal: matidez en flancos que además se cambia al rotar al pacienteSi ↑PVY orienta a ICC ó Pericarditis constrictiva como causa de ascitis ( o al menos una de las causas)


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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISExploración física

Pacientes alcohólicos con miocardiopatia dilatada enólica y ascitis, se les infradiagnostica frecuentemente la ICC: en eco se ve ascitis y se etiqueta de cirrosis sin estar presente: importante distinción por distintas implicaciones terapéuticas.Nódulo (umbilical) de la hermana MªJosé: cáncercomo causa de la ascitis: gástrico, cólon, hepatocelular, linfoma (AP da Dx)


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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISDiagnóstico

Exploración fisica: S:50-94% y E: 29-82% comparados con el gold standard: eco abdominalTres grados de ascitis: 1 LEVE(solo detectable por eco), 2 MODERADA (distensión simétrica mod abd) y 3 SEVERA (marcada distensión abd): 1+ a 4+(masiva y a tensión)Matidez en flancos: 1500mlEco abdominal: 100-150ml detecta. Ver higado y bazo: si ≥12 cm ó recanalizacion v.umbilical →evidencia indirecta de HTP. Detecta obstrucc biliar, hepatocarcinomaParacentesis: confirma ascitis, dx etiologia y dx si hay infección


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Indications for abdominal paracentesis in a patient with ascitesNew onset ascites

At the time of each admission to the hospital

Clinical deterioration, either inpatient or outpatient

Fever

Abdominal pain

Abdominal tenderness

Mental status change

Ileus

Hypotension

Laboratory abnormalities that may indicate infection

Peripheral leukocytosis

Acidosis

Worsening of renal function

Gastrointestinal bleeding (a high risk time for infection)


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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISParacentesis Diagnóstica

Apariencia, transparencia, turbidez, lechoso (ascitis quilosa: causa + frec: neo/cirrosis/traumatismo linfaticos) rosado(>10000 eritrocitos/mm3), rojo (>>10000 eritrocitos/mm3)Iniciar atb empirico si neutrofilos ≥250/mm3

Sangrado traumatico: heterogeneo, no traumatico es homogéneoAscitis hemorrágica: fuga por pinchazo de colateral, cirrosis, cancer(hepatocarcinoma pueden desarrollar un sangrado masivo intraabdominal)TBC peritoneal raramente es hemorragicaAscitis marron: y Bilirrubina es mayor q la sérica: ulcera duodenal perforada o rotura vesicula


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DIAGNÓSTICO DIFERENCIAL DE LA ASCITISLíquido ascítico

Esta infectado? Nº célulasHay HTP?

Gradiente Albúmina sérica-Albúmina ascítica

El nº de células en liquido ascítico nos hará tomar decisiones de vida o muerte por ello es

imprescindible tener el resultado cuanto antes: si el liquido esta infectado y no ponemos atb el

paciente puede fallecer


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En ICC y ascitis el gradiente As-Aa puede estrecharse pero en cirrosis permanece estable a

no ser que baje la TA mucho


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¿Cultivos? Si en ascitis de inicio, deterioro (fiebre, dolor abdominal, azoemia, acidosis o confusion) no necesario en paracentesis terapéuticas y sin

síntomas/signos de infección¿Cómo? 10ml de liquido ascítico mejor en

frascos de hemocultivos


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ProteinasProteinas totales<1 g/dL: alto riesgo de PBE: dar atb selectivos para prevenir

GlucosaGlucosa baja por consumo de bacterias y tb en carcinomatosis peritoneal, indetectable en

perforacion intestinal al l.ascitico


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LEUCOCITOSLIQUIDO ASCITICO

<500

≥500

<250 PMN

≥250 PMN

≥1.1 GRADIENTE As-Aa : HTP

<1.1 GRADIENTEAs-Aa: no HTP

≥50% PMN

<50%PMN

≥1.1 GRADIENTEAs-Aa : HTP

<1.1 GRADIENTE As-Aa: no HTP

<1.1 GRADIENTEAs-Aa: no HTP

≥1.1 GRADIENTEAs-Aa : HTP

<2,5g/dL PT en L.A.

≥2,5g/dL PT en L.A.

<2,5g/dL PT en L.A.

cultivo + 1 microorg<1g/dLPTGluc>50mg/dL, LDH<225

Polimicrob, PT>1g/dL, Gluc<50, LDH≥225

Amilasa L.A.>100

Citologia +

Enviar cultivo micobacterias

Citologia +

Enviar cultivo micobacterias


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Ascitis cirrótica no complicadaAscitis cardiacaAscitis nefróticaPeritonitis bacteriana espontaneaPeritonitis bacteriana secundariaAscitis pancreáticaCarcinomatosis peritoneal con HTPPeritonitis TBC con cirrosis de baseCarcinomatosis peritonealPeritonitis TBC


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Eco abdominal y/o bx hepáticaRx tórax y ecocardiogramaProteinuria de 24hRespuesta clínica a antibióticosEstudios contraste hidrosoluble intestinal(enema opaco)TAC abdominalBúsqueda de tumor primarioBx peritoneal laparoscopica y cultivo micobacterias

Cirugia si se documenta perforacion intestinal

tuberculostaticos


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American Association for the Study of Liver Diseases (AASLD) recommendations for the management of adult patients with ascites due to cirrhosisascites due to cirrhosis

1.Evaluation and diagnosis

Abdominal paracentesis should be performed and ascitic fluid should be obtained from inpatients and outpatients with clinically apparent new‐onset ascites.

Because bleeding is sufficiently uncommon, the routine prophylactic use of fresh frozen plasma or platelets before paracentesis is not recommended.

Data from: Runyon BA. Management of adult patients with ascites due to cirrhosis: an update. Hepatology 2009; 49:2087.


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2.Differential diagnosis

The initial laboratory investigation of ascitic fluid should include an ascitic fluid cell count and differential, ascitic fluid total protein, and serum‐ascites albumin gradient (SAAG).

If ascitic fluid infection is suspected, ascitic fluid should be cultured at the bedside in blood culture bottles prior to initiation of antibiotics.

Other studies of ascitic fluid can be ordered based on pretest probability of disease.

Testing serum for CA125 is not helpful in the differential diagnosis of ascites. Its use is not recommended in patients with ascites of any type.


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Routine testsCell count and differentialAlbumin concentrationTotal protein concentrationCulture in blood culture bottles

Optional testsGlucose concentrationLDH concentrationGram stainAmylase concentration

Unusual testsTuberculosis smear and cultureCytologyTriglyceride concentrationBilirubin concentration


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3.Treatment of ascitesPatients with ascites who are thought to have an alcohol component to their liver injury should abstain from alcohol consumption.

Firstline treatment of patients with cirrhosis and ascites consists of sodium restriction (88 mmol/day [2000 mg/day]) and diuretics (oral spironolactone with or without oral furosemide).

Fluid restriction is not necessary unless serum sodium is less than 120 to 125 mmol/L.

An initial therapeutic abdominal paracentesis should be performed in patients with tense ascites. Sodium restriction and oral diuretics should then be initiated.

Diuretic‐sensitive patients should preferably be treated with sodium restriction and oral diuretics rather than with serial paracenteses.

Liver transplantation should be considered in patients with cirrhosis and ascites.


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CT scan shows a large volume of ascitic fluid surrounding a small shrunken cirrhotic liver. The fluid is of low attenuation and is free floating without septations or solid material.Courtesy of Jonathan Kruskal, MD.


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5.Hepatorenal syndromeAlbumin infusion plus administration of vasoactive drugs such as octreotide and midodrine should be considered in the treatment of type I hepatorenal syndrome.Patients with cirrhosis, ascites, and type I hepatorenal syndrome should have an expedited referral for liver transplantation.


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6.Spontaneous bacterial peritonitis (SBP)Patients with ascites admitted to the hospital should undergo abdominal paracentesis. Paracentesis should be repeated in patients (whether in the hospital or not) who develop signs or symptoms or laboratory abnormalities suggestive of infection (eg, abdominal pain or tenderness, fever, encephalopathy, renal failure, acidosis, or peripheral leukocytosis).

Patients with ascitic fluid PMN counts ≥250 cells/mm3 (0.25 X 109/L) should receive empiric antibiotic therapy, eg, an intravenous third‐generation cephalosporin, preferably cefotaxime 2 g every 8 hours.

Oral ofloxacin (400 mg twice per day) can be considered a substitute for intravenous cefotaxime in inpatients without prior exposure to quinolones, vomiting, shock, grade II (or higher) hepatic encephalopathy, or serum creatinine >3 mg/dL.

Patients with ascitic fluid polymorphonuclear leukocyte (PMN) counts <250 cells/mm3 (0.25 X 109/L) and signs or symptoms of infection (temperature >100°F or abdominal pain or tenderness) should also receive empiric antibiotic therapy, eg, intravenous cefotaxime 2 g every 8 hours, while awaiting results of cultures.When the ascitic fluid of a patient with cirrhosis is found to have a PMN count ≥250 cells/mm3 (0.25 X 109/L) and there is high suspicion of secondary peritonitis, it should also be tested for total protein, LDH, glucose, Gram stain, carcinoembryonic antigen, and alkaline phosphatase to assist with the distinction of SBP from secondary peritonitis.

Patients with ascitic fluid PMN counts ≥250 cells/mm3 (0.25 X 109/L) and clinical suspicion of SBP, who also have a serum creatinine >1 mg/dL, blood urea nitrogen >30 mg/dL, or total bilirubin >4 mg/dL should receive 1.5 g albumin/kg body weight within 6 hours of detection and 1.0 g/kg on day 3.


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7.Prevention of spontaneous bacterial peritonitisIntravenous ceftriaxone for 7 days or twice‐daily norfloxacin for 7 days should be given to prevent bacterial infections in patients with cirrhosis and gastrointestinal hemorrhage.

Patients who have survived an episode of SBP should receive long‐term prophylaxis with daily norfloxacin (or trimethoprim/sulfamethoxazole) because this is the most data‐supported indication for long‐term outpatient prophylaxis.

In patients with cirrhosis and ascites but no gastrointestinal bleeding, long‐term use of norfloxacin (or trimethoprim/sulfamethasoxazole) can be justified if the ascitic fluid protein <1.5 g/dL and at least one of the following is present: serum creatinine ≥1.2 mg/dL, blood urea nitrogen ≥25 mg/dL, serum sodium ≤130 mEq/L, or Child‐Pugh ≥9 points with bilirubin ≥3 mg/dL.

Intermittent dosing of antibiotics to prevent bacterial infections may be inferior to daily dosing (due to the development of bacterial resistance) and thus daily dosing should preferentially be used.


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BIBLIOGRAFÍAUpToDate:• Diagnosis and evaluation of patients with ascites, Bruce A Runyon, MD,

Marshall M Kaplan, MDPeter A L Bonis, MD, last updated: nov 16, 2011. • Initial therapy of ascites in patients with cirrhosis, José Such, MD, PhD,

Bruce A Runyon, MD, Marshall M Kaplan, MD, Peter A L Bonis, MD, last updated: abr 25, 2011

• Treatment of diuretic‐resistant ascites in patients with cirrhosis, José Such, MD, PhD Bruce A Runyon, MD Paul Angulo, MD Peter A L Bonis, MD,last updated: abr 27, 2012.

• Malignancy‐related ascites, Bruce A Runyon, MD, Lawrence S Friedman, MD, Peter A L Bonis, MD, last updated: jun 9, 2010

• Chylous, bloody, and pancreatic ascites Andrés Cárdenas, MD, MMSc, AGAF, Andres Gelrud, MD, Sanjiv Chopra, MD, Bruce A Runyon, MD, Anne C Travis, MD, MSc, FACG, last updated: abr 17, 2012.


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BIBLIOGRAFÍA

• Varios Autores. Manual CTO Medicina y Cirugía, 7ª Edición, Tomo I, 330‐337, y Adenda.

• Harrison's principles of internal medicine, 18th Edition, Part , Section , Chapter :

• Martín Asenjo, R., Bastante Valiente, M.T., Torres Macho, J. Manual de diagnóstico y Terapéutica Médica. H.U. 12 de Octubre, 6ª Edición,

• Jiménez Murillo, L., Montero Pérez, F.J., Guía Terapéutica. Medicina de Urgencias, 3ª Edición,

• De Castro Del Pozo, S. Manual de Patología General, 5ª Edición,


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VALORACIÓN FUNCIONAL DE LA CIRROSIS: CLASIFICACIÓN DE CHILD‐PUGH

PARÁMETRO GRADO 1 GRADO 2 GRADO 3

EPH No 1 a 2 3 a 4

ASCITIS Ausente Ligera Moderada

BILIRRUBINA(mg/dl) 1 a 2 2 a 3 >3

ALBÚMINA (g/l) >35 28 a 35 <28

ACTIVIDAD DE PROTROMBINA

>50% 30‐50% <30%

CHILD‐PUGHA (Leve) 5 ‐ 6 CIRUGÍA

B 7 ‐ 9 TIPS

C 10 ‐ 15 TIPS


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GRACIAS A TODOS


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DIAGNÓSTICO DIFERENCIAL Y MANEJO DE LA ASCITIS · PDF fileVer higado y bazo: si ≥12...

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