How should shock state from hepatic causes be managed?

Management of Shock State from Hepatic Causes

In patients with shock from hepatic causes (cirrhosis/ACLF), use norepinephrine as first-line vasopressor targeting MAP ≥65 mmHg, add vasopressin as second-line agent, resuscitate with balanced crystalloids or albumin (select indications), and consider hydrocortisone 50 mg IV q6h for refractory shock requiring high-dose vasopressors. 1

Initial Assessment and Hemodynamic Monitoring

• Perform early baseline assessment of volume status, perfusion, and cardiovascular function in all critically ill cirrhotic patients with shock. 1

• Utilize bedside echocardiography to evaluate volume status and cardiac function in patients with cirrhosis and hypotension or shock. 1 This helps distinguish between hypovolemic, cardiogenic, and vasodilatory components.

• Implement invasive hemodynamic monitoring (arterial and central venous catheter) for adequate assessment of cardiac function and titration of vasopressors and fluid resuscitation. 1

Fluid Resuscitation Strategy

• Use a judicious strategy for intravascular volume resuscitation utilizing hemodynamic monitoring tools to optimize volume status. 1

• Administer balanced crystalloids (e.g., lactated Ringer's) and/or albumin for fluid administration if resuscitation is required. 1 Albumin is specifically indicated for select liver-related conditions but its broader use as a general resuscitation agent in critically ill cirrhotic patients is not well-defined. 1

• Avoid aggressive fluid overload as cirrhotic patients are prone to pulmonary edema and ascites accumulation. 1

Vasopressor Management

First-Line Vasopressor

• Initiate norepinephrine (0.01–0.5 μg/kg/min) as the first-line vasopressor to maintain adequate organ perfusion pressure with concurrent appropriate fluid resuscitation. 1 This recommendation is based on general septic shock guidelines as trials specifically in cirrhosis/ACLF are lacking. 1

• Target a MAP of 65 mm Hg in patients with cirrhosis and septic shock with ongoing assessment of end-organ perfusion (mental status, capillary refill, urine output, extremity perfusion, lactate, central venous oxygen saturation). 1 While a retrospective study of 273 critically ill cirrhotic patients suggested maintaining MAP >65 mmHg, 1 patients with cirrhosis generally have lower baseline MAP and individualized targets based on end-organ perfusion are appropriate. 1

Second-Line Vasopressor

• Add vasopressin as a second-line agent when increasing doses of norepinephrine are required. 1 Vasopressin deficiency has been documented in cirrhosis as well as in many shock states. 1

• Be aware that vasopressin is associated with lower incidence of tachyarrhythmias but higher rate of digital ischemia compared to other vasoactive agents. 1

Alternative Vasopressor for Hepatorenal Syndrome

• Consider norepinephrine as an alternative to terlipressin for patients with hepatorenal syndrome (HRS-AKI) and may be preferred in patients with shock. 1 Meta-analyses show no difference in reversibility or relapse of HRS between terlipressin + albumin and norepinephrine + albumin arms. 1

Management of Refractory Shock and Adrenal Insufficiency

• Consider screening for adrenal insufficiency or an empiric trial of hydrocortisone 50 mg IV q6h or 200-mg infusion for 7 days or until ICU discharge for treatment of refractory shock requiring high-dose vasopressors. 1

• Recognize that relative adrenal insufficiency (increase in serum cortisol <9 μg/dL after Synacthen administration) is common in cirrhotic patients (49% prevalence) and is associated with significantly higher 90-day mortality (26% vs. 10%, p=0.008). 1

• Hydrocortisone is recommended based on the ADRENAL and APROCCHSS trials, which documented earlier shock reversal and potential mortality benefit. 1 However, specific studies in ACLF patients are small with variable impact on mortality. 1

• Monitor for increased risk of gastrointestinal bleeding with hydrocortisone use in cirrhotic patients. 1

Infection Management

• Perform systematic search for infection including microbiological and cytological examination of ascites fluid (polymorphonuclear cells >250/mm³ confirms spontaneous bacterial peritonitis). 1

• Initiate early empirical antibiotic therapy tailored to the suspected site of infection, causative pathogen, and local ecology. 1 Infection is the most common precipitant of ACLF (48% prevalence) and delayed antibiotic therapy is associated with significantly increased mortality. 1

Critical Pitfalls to Avoid

• Do not confuse hepatorenal syndrome with shock state. HRS diagnostic criteria specifically require "absence of shock" as one of the criteria. 1 If shock is present, the primary management is vasopressors for shock, not terlipressin for HRS.

• Avoid using terlipressin in patients with ACLF-3 (EASL-CLIF) or major cardiopulmonary or vascular disease as it is contraindicated in these settings. 1

• Do not delay vasopressor initiation waiting for central venous access - start vasopressors peripherally to restore MAP rather than delaying. 1

• Recognize that fever is often absent in cirrhotic patients with sepsis, making infection diagnosis challenging. 1 Look for new or worsening decompensation (worsening mental status, hyponatremia, AKI, relative increase in WBC count, change in hemodynamics). 1

Distinguishing Shock Liver from Cirrhotic Shock

• Shock liver (ischemic hepatitis) presents with sudden elevation of transaminases to >20 times upper limit of normal following cellular anoxia, with resolution to near normal within 7-10 days. 2, 3 This is distinct from shock in a patient with pre-existing cirrhosis.

• In shock liver, management focuses on stabilization of cardiac output to improve hepatic perfusion and optimization of liver oxygenation. 2, 4, 5 The underlying precipitating cause (cardiac failure, sepsis, hypotension) must be rapidly identified and treated. 2, 3