How to manage shock in a patient with chronic liver disease (CLD) without evidence of hypovolemic, septic, or obstructive shock?

Management of Shock in Chronic Liver Disease Without Hypovolemic, Septic, or Obstructive Causes

In a CLD patient with shock of unclear etiology after excluding hypovolemia, sepsis, and obstruction, you are likely dealing with vasodilatory shock from the hyperdynamic circulatory state of cirrhosis itself, potentially complicated by relative adrenal insufficiency or cirrhotic cardiomyopathy—manage with norepinephrine as first-line vasopressor, consider empiric hydrocortisone for refractory shock, and use bedside echocardiography to guide therapy. 1

Initial Assessment and Hemodynamic Characterization

Perform immediate bedside echocardiography to differentiate between vasodilatory shock (hyperdynamic circulation with high cardiac output and low systemic vascular resistance), cirrhotic cardiomyopathy (reduced contractility), or portopulmonary hypertension with right ventricular dysfunction. 1 This is critical because patients with decompensated cirrhosis characteristically demonstrate a hyperdynamic circulation with decreased systemic vascular resistance, low arterial blood pressure, and increased cardiac output, which is exacerbated with worsening inflammation in ACLF. 1, 2

Assess volume status comprehensively using:

• Physical examination (capillary refill, extremity perfusion, mental status) 1
• Echocardiographic evaluation of inferior vena cava and cardiac preload 1
• Dynamic hemodynamic monitoring with stroke volume variation, pulse pressure variation, or passive leg raise testing 1
• End-organ perfusion markers (urine output, lactate, central venous oxygen saturation) 1

Vasopressor Management

Initiate norepinephrine (0.01–0.5 μg/kg/min) as the first-line vasopressor to maintain adequate organ perfusion pressure, targeting a MAP of 65 mm Hg with ongoing assessment of end-organ perfusion. 1 Start vasopressors peripherally rather than delaying for central access. 1

Add vasopressin as a second-line agent when increasing doses of norepinephrine are required. 1 Vasopressin deficiency is documented in cirrhosis and may be particularly relevant in this population. 1 Be aware that vasopressin carries a higher rate of digital ischemia compared to other vasoactive agents, though it has lower incidence of tachyarrhythmias. 1

Establish invasive arterial monitoring as soon as practical for accurate blood pressure measurement and frequent assessment, as the hyperdynamic state in cirrhosis may bias accuracy of non-invasive monitoring. 1, 2

Addressing Relative Adrenal Insufficiency

Consider empiric hydrocortisone 50 mg IV every 6 hours (or 200-mg continuous infusion) for refractory shock requiring high-dose vasopressors. 1 Relative adrenal insufficiency occurs in 49% of patients with cirrhosis and acute decompensation, and is associated with significantly higher 90-day mortality (26% vs. 10%, p = 0.008). 1

The ADRENAL and APROCCHSS trials documented earlier shock reversal and potential mortality benefit with hydrocortisone in refractory shock. 1 Continue treatment for 7 days or until ICU discharge. 1

Screening for adrenal insufficiency (cortisol increase <9 μg/dL after Synacthen administration) can be performed, though empiric treatment is reasonable in refractory shock. 1

Judicious Fluid Management

Use balanced crystalloids (lactated Ringer's) as first-line fluid if any volume resuscitation is needed. 1 Balanced crystalloids limit the risk of hyperchloremic acidosis and subsequent adverse kidney events. 2

Albumin may be considered in select indications but use cautiously to avoid volume overload. 1 While albumin has beneficial properties beyond volume expansion in cirrhosis (anti-inflammatory, oncotic), excessive use can precipitate pulmonary edema and respiratory failure. 3, 4 The ATTIRE trial demonstrated that maintaining elevated albumin levels in decompensated cirrhosis was associated with higher rates of pulmonary edema. 3, 4

Monitor fluid responsiveness continuously using dynamic hemodynamic parameters rather than static measures, as overresuscitation is particularly harmful in cirrhosis. 1

Monitoring and Titration Strategy

Target MAP of 65 mm Hg but individualize based on frequent assessment of end-organ perfusion rather than rigid adherence to a single number. 1 Patients with cirrhosis generally have lower baseline MAP. 1

Establish central venous access for central venous oxygen saturation monitoring and reliable vasopressor delivery once initial stabilization is achieved. 1

Monitor for complications specific to cirrhosis:

• Hepatopulmonary syndrome or portopulmonary hypertension affecting oxygenation 1
• Right ventricular dysfunction in the setting of portopulmonary hypertension 1
• Worsening hepatic encephalopathy from hypoperfusion 1

Key Pitfalls to Avoid

Do not delay vasopressor initiation while pursuing central access—peripheral administration is acceptable initially. 1

Avoid excessive fluid administration as the hyperdynamic circulation in cirrhosis does not necessarily indicate hypovolemia; use dynamic assessments to guide therapy. 1, 2

Do not use albumin as routine resuscitation fluid outside specific liver-related indications (large-volume paracentesis, spontaneous bacterial peritonitis, hepatorenal syndrome), as it increases pulmonary edema risk. 3, 4

Recognize that standard critical care hemodynamic targets may not apply—the baseline hyperdynamic state and low systemic vascular resistance in liver failure may bias accuracy of some monitoring devices. 2