DIAGNÓSTICO DIFERENCIAL Y MANEJO DE LA ASCITIS
MARI CRUZ PÉREZ PANIZO MIR MEDICINA INTERNA
COMPLEJO ASISTENCIAL UNIVERSITÁRIO DE LEÓN 11-6-2012
SESIONES BIBLIOGR
SESIONES BIBLIOGRÁFICAS RESIDENTESÁFICAS RESIDENTES
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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Causas
-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 percent
Cancer 10 percent
Heart failure 3 percent Tuberculosis 2 percent
Dialysis 1 percent
Pancreatic disease 1 percent
Other 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
Rare causes of ascites
Hematologic
Amyloidosis
Castleman's syndrome
Extramedullary hematopoiesis Hemophagocytic syndrome Histiocytosis X
Leukemia Lymphoma
Multiple myeloma
Rare causes of ascites
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 HEP
CIRROSIS HEPÁTICA:ÁTICA:
1.COMPLICACIONES POR LA HTPORTAL:
-HDA POR VARICES ESOFÁGICAS O POR GASTROPATÍA DE LA HTP
-ASCITIS: ES LA COMPLICACIÓN MÁS FRECUENTE
-EPH
2.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 diabética
Complicaciones obesidad: nefropatia diabética + ICC + cirrosis debida a Esteatohepatitis no alcohólica
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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Exploración 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.
Ictericia
Pérdida de masa muscular
Leuconiquia: uñas de Muehrcke, Terry
Hipertrofia 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 hepatocarcinoma
Principal: matidez en flancos que además se cambia al rotar al paciente
Si ↑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 ASCITIS Exploración 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: cáncer como causa de la ascitis: gástrico, cólon,
hepatocelular, linfoma (AP da Dx)
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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Diagnóstico
Exploración fisica: S:50-94% y E: 29-82%
comparados con el gold standard: eco abdominal Tres 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: 1500ml
Eco abdominal: 100-150ml detecta. Ver higado y bazo: si ≥12 cm ó recanalizacion v.umbilical
→evidencia indirecta de HTP. Detecta obstrucc biliar, hepatocarcinoma
Paracentesis: confirma ascitis, dx etiologia y dx si hay infección
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Indications for abdominal paracentesis in a patient with ascites
New 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 ASCITIS Paracentesis Diagnóstica
Apariencia
, transparencia, turbidez, lechoso (ascitis quilosa: causa + frec: neo/cirrosis/traumatismo linfaticos) rosado(>10000eritrocitos/mm3), rojo (>>10000 eritrocitos/mm3) Iniciar atb empirico si neutrofilos ≥250/mm3
Sangrado traumatico: heterogeneo, no traumatico es homogéneo Ascitis hemorrágica: fuga por pinchazo de colateral, cirrosis,
cancer(hepatocarcinoma pueden desarrollar un sangrado masivo intraabdominal)
TBC peritoneal raramente es hemorragica
Ascitis marron: y Bilirrubina es mayor q la sérica: ulcera duodenal perforada o rotura vesicula
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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Líquido ascítico
Esta infectado? Nº células Hay 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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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Líquido ascítico
Esta infectado? Nº células Hay HTP?
Gradiente Albúmina sérica-Albúmina ascítica 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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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Líquido ascítico
Esta infectado? Nº células Hay HTP?
Gradiente Albúmina sérica-Albúmina ascítica
¿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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DIAGNÓSTICO DIFERENCIAL DE LA ASCITIS Líquido ascítico
Esta infectado? Nº células Hay HTP?
Gradiente Albúmina sérica-Albúmina ascítica Proteinas
Proteinas totales<1 g/dL: alto riesgo de PBE: dar atb selectivos para prevenir
Glucosa
Glucosa baja por consumo de bacterias y tb en carcinomatosis peritoneal, indetectable en
perforacion intestinal al l.ascitico
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LEUCOCITOS LIQUIDO
ASCITICO
<500
≥500
<250 PMN
≥250 PMN
≥1.1 GRADIENTE As-Aa : HTP
<1.1 GRADIENTE As-Aa: no HTP
≥50% PMN
<50%PMN
≥1.1 GRADIENTE As-Aa : HTP
<1.1 GRADIENTE As-Aa: no HTP
<1.1 GRADIENTE As-Aa: no HTP
≥1.1 GRADIENTE As-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/dLPT
Gluc>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 complicada Ascitis cardiaca
Ascitis nefrótica
Peritonitis bacteriana espontanea Peritonitis bacteriana secundaria Ascitis pancreática
Carcinomatosis peritoneal con HTP
Peritonitis TBC con cirrosis de base
Carcinomatosis peritoneal Peritonitis TBC
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Eco abdominal y/o bx hepática Rx tórax y ecocardiograma
Proteinuria de 24h
Respuesta clínica a antibióticos Estudios contraste hidrosoluble intestinal(enema opaco)
TAC abdominal
Búsqueda de tumor primario Bx 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 tests
Cell count and differential Albumin concentration
Total protein concentration
Culture in blood culture bottles
Optional tests
Glucose concentration LDH concentration
Gram stain
Amylase concentration
Unusual tests
Tuberculosis smear and culture Cytology
Triglyceride concentration Bilirubin concentration
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3.Treatment of ascites
Patients 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 syndrome
Albumin 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 peritonitis
Intravenous 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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BIBLIOGRAFÍA
UpToDate:
• 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‐PUGH
A (Leve) 5 ‐ 6 CIRUGÍA
B 7 ‐ 9 TIPS
C 10 ‐ 15 TIPS
