Manejo de la Hipotensión en Pacientes Cirróticos

Evaluación inicial

• Realizar una evaluación temprana del estado de volumen, perfusión y función cardiovascular en todos los pacientes cirróticos con hipotensión 1
• Utilizar ecocardiografía a la cabecera del paciente para evaluar el estado de volumen y la función cardíaca, lo que ayudará a distinguir entre shock hipovolémico, vasodilatador o cardiogénico 2
• Monitorizar los cambios dinámicos en el volumen sistólico, variación del volumen sistólico, variación de la presión del pulso durante la resucitación con fluidos 1

Resucitación con fluidos

• Utilizar cristaloides balanceados (como Ringer lactato) como primera línea para la resucitación con fluidos en pacientes cirróticos con hipotensión 1
• Los cristaloides balanceados se asocian con menor mortalidad en comparación con solución salina en pacientes críticos 1
• La albúmina está indicada en situaciones específicas relacionadas con la cirrosis, como paracentesis de gran volumen (>5L): administrar 8g de albúmina por litro de ascitis extraída 3
• En pacientes con cirrosis e hipotensión inducida por sepsis, la albúmina al 20% logra una reversión más rápida de la hipotensión en comparación con cristaloides 1
• Un estudio aleatorizado mostró que la albúmina al 5% en comparación con solución salina normal en pacientes con cirrosis e hipotensión inducida por sepsis logró mayor supervivencia a una semana (43.5% vs. 38.3%) 1

Vasopresores

• La norepinefrina es el vasopresor de primera línea para pacientes con hipotensión, con resucitación con fluidos concurrente 1, 4
• La vasopresina se recomienda como agente de segunda línea cuando se requieren dosis crecientes de norepinefrina 4, 5

Objetivos de presión arterial

• Mantener una presión arterial media (PAM) objetivo de 65 mmHg en pacientes con cirrosis y shock séptico 1, 4
• Un estudio observacional retrospectivo de 273 pacientes cirróticos críticamente enfermos informó que la mortalidad en UCI aumentó por debajo de un umbral de 65 mmHg 1

Insuficiencia suprarrenal relativa

• La insuficiencia suprarrenal relativa es común en pacientes con cirrosis y se asocia con mayor mortalidad y complicaciones 4, 5
• Considerar la detección de insuficiencia suprarrenal o un ensayo empírico de hidrocortisona 50 mg IV cada 6 horas o infusión de 200 mg durante 7 días o hasta el alta de la UCI para el tratamiento del shock refractario que requiere vasopresores en dosis altas 4

Consideraciones especiales

• La restricción de líquidos no es necesaria en la mayoría de los pacientes con cirrosis y ascitis 6
• La hiponatremia severa (sodio sérico <125 mmol/L) justifica la restricción de líquidos a 1-1.5 L/día en pacientes con cirrosis que están clínicamente hipervolémicos 7
• La administración de cloruro de sodio hipertónico (3%) debe reservarse para aquellos que están gravemente sintomáticos con hiponatremia aguda, y el sodio sérico debe corregirse lentamente 7

Complicaciones y pitfalls a evitar

• Evitar la sobrecorrección rápida de la hiponatremia con solución salina hipertónica, ya que puede provocar más complicaciones que la hiponatremia en sí 6
• Los inhibidores de la enzima convertidora de angiotensina han demostrado agravar la hipotensión y no han sido clínicamente útiles 6

Circulatory Dysfunction in Decompensated Cirrhosis

Pathophysiology and Diagnosis

• Patients with decompensated cirrhosis typically present with a hyperdynamic circulation characterized by high cardiac output and low systemic vascular resistance, according to the European Association for the Study of the Liver 8, 9
• Cirrhotic cardiomyopathy (CCM) prevents adequate cardiac output compensation in advanced decompensation, leading to effective hypovolemia despite the typical hyperdynamic state, as noted by the European Association for the Study of the Liver 8
• Cold extremities indicate peripheral vasoconstriction, which is atypical for pure vasodilatory shock and suggests either severe hypovolemia, cardiogenic component from CCM, or mixed shock with inadequate cardiac compensation, as reported by the American Association for the Study of Liver Diseases 8, 9

Management

• The European Association for the Study of the Liver guidelines define failure to control bleeding as development of hypovolemic shock, and recommend immediate assessment for active bleeding and volume resuscitation 10
• Bedside echocardiography is essential to distinguish between hypovolemic, vasodilatory, and cardiogenic shock, and to assess left ventricular and right ventricular function, evaluate inferior vena cava for volume status, and determine fluid responsiveness with stroke volume variation, as recommended by the American Association for the Study of Liver Diseases 9
• Target mean arterial pressure (MAP) of 65 mmHg, and use norepinephrine as the first-line vasopressor with concurrent fluid resuscitation, as suggested by the European Association for the Study of the Liver 9, 11
• Avoid rapid correction of hyponatremia if present, to prevent central pontine myelinolysis, as warned by the European Association for the Study of the Liver 12

Pathophysiology of Hypovolemic Shock from Third Spacing in Decompensated Liver Cirrhosis

The Paradox: Fluid Overload with Effective Hypovolemia

• Splanchnic arterial vasodilation is the primary driver of the paradoxical state of total extracellular fluid overload but central effective circulating hypovolemia in patients with decompensated cirrhosis, caused by portal hypertension and increased circulating vasodilators, according to the European Association for the Study of the Liver 13, 14
• Portal hypertension acts as a compartmentalizing factor, trapping expanded extracellular fluid volume in the peritoneal cavity and splanchnic circulation rather than maintaining effective central blood volume, as stated by the American Association for the Study of Liver Diseases 13
• Activation of sodium-retaining systems in response to perceived hypovolemia worsens ascites formation in patients with decompensated cirrhosis, as reported by the European Association for the Study of the Liver 13

The Role of Inflammation and Microcirculatory Dysfunction

• Increased circulating pro-inflammatory cytokines and chemokines play a direct role in organ dysfunction in patients with decompensated cirrhosis, according to the American Association for the Study of Liver Diseases 14, 15
• Synergic interplay of inflammation and microvascular dysfunction amplifies cellular injury signals in patients with decompensated cirrhosis, as stated by the European Association for the Study of the Liver 14, 15
• Mitochondria-mediated metabolic downregulation in tubular cells causes them to prioritize survival over normal function, sacrificing sodium/chloride absorption and triggering further RAAS activation that lowers GFR in patients with decompensated cirrhosis, as reported by the American Association for the Study of Liver Diseases 15

Third Spacing Mechanics in This Context

• Ascites accumulation results from renal sodium retention due to RAAS activation, with the positive fluid balance leading to extracellular fluid volume expansion that preferentially accumulates in the peritoneal cavity in patients with decompensated cirrhosis, as stated by the European Association for the Study of the Liver 13
• Reduced effective volaemia secondary to splanchnic arterial vasodilation is the main determinant of third spacing in patients with decompensated cirrhosis, but renal function abnormalities induced by systemic inflammation also play a role, especially in advanced stages, according to the American Association for the Study of Liver Diseases 13

Dyspnea Pathophysiology

• Ascites-induced restrictive ventilatory dysfunction from massive abdominal distension contributes to dyspnea in patients with decompensated cirrhosis, as reported by the European Association for the Study of the Liver 13
• Hepatic hydrothorax from transdiaphragmatic fluid movement causes restrictive ventilatory dysfunction and contributes to dyspnea in patients with decompensated cirrhosis, according to the American Association for the Study of Liver Diseases 13