Can hypoglycemia (low blood sugar) cause shock liver (hepatic ischemia)?

From the Guidelines

Hypoglycemia can indeed cause shock liver, as it can lead to decreased cardiac output and hypotension, reducing blood flow to the liver and resulting in hepatocyte damage. This condition is a concern in clinical practice, particularly in patients with acute liver failure, where hypoglycemia is a common problem due to the loss of hepatic gluconeogenetic capacity, lack of glycogen, and hyperinsulinism 1. According to the ESPEN guidelines on parenteral nutrition, sufficient glucose provision is mandatory for the prophylaxis and treatment of hypoglycemia, with a recommended intake of 2-3 g kg-1 d-1 1.

Key points to consider in the management of hypoglycemia to prevent shock liver include:

• Prompt treatment of hypoglycemia with glucose administration, typically using D50W for severe cases, followed by D10W infusion
• Maintaining adequate blood pressure and supporting cardiac function
• Monitoring liver function tests during recovery, which typically shows improvement within days if the underlying cause is corrected
• Ensuring euglycaemia, as strict blood glucose control has been shown to confer a survival and morbidity benefit to critically ill patients, regardless of etiology 1

It is essential to note that the oxidation of fatty acids and ketogenesis are the main energy-yielding processes for hepatocytes, and adequate provision of lipid may be a plausible therapeutic objective, provided there is sufficient oxygen supply to the hepatic tissue 1. However, in cases of acute liver failure with microvesicular steatosis and mitochondrial dysfunction, exogenous lipid may be harmful, and its use should be approached with caution 1.

From the Research

Hypoglycemia and Shock Liver

• Hypoglycemia can be a complication of shock liver, also known as hypoxic hepatitis or ischemic hepatitis, as stated in 2, 3, 4.
• Shock liver is characterized by centrilobular liver cell necrosis and sharply increasing serum aminotransferase levels in a clinical setting of cardiac, circulatory, or respiratory failure 2.
• Hypoglycemia is considered secondary to reduced gluconeogenesis in the exhausted liver, as mentioned in 3.
• The relationship between hypoglycemia and shock liver is complex, and hypoglycemia can be both a cause and a consequence of liver injury, as suggested in 5.

Pathophysiology and Clinical Management

• The pathophysiology of shock liver involves hepatic congestion from right heart failure, reduced hepatic blood flow, total body hypoxemia, reduced oxygen uptake by hepatocytes, or reperfusion injury following ischemia, as explained in 4.
• The diagnosis of shock liver is primarily clinical and typically does not require liver biopsy, as stated in 4.
• The definitive treatment of shock liver involves correction of the underlying disease state, but successful management includes monitoring for potential complications such as hypoglycemia, hyperglycemia, hyperammonemia, and hepatopulmonary syndrome, as mentioned in 4.

Clinical Implications

• Hypoglycemia is a common phenomenon in patients with various severe liver diseases, including acute on chronic liver failure, as reported in 6.
• Patients with cirrhosis, a higher model for end-stage liver disease (MELD) score, and a significant decrease in fibrinogen are more likely to develop hypoglycemia, as found in 6.
• The 90-day mortality rate in patients with hypoglycemia is significantly higher than in those without hypoglycemia, as shown in 6.