Despite continuous progress in medicine, sepsis remains the main cause of deaths in the intensive care unit. Liver failure complicating sepsis/septic shock has a significant impact on mortality in this group of patients. The pathophysiology of sepsis-associated liver dysfunction is very complicated and still not well understood. According to the Surviving Sepsis Campaign (SSC) Guidelines, the diagnosis of liver dysfunction during sepsis is based on the increase in bilirubin concentration >2 mg/dL and the occurrence of coagulation disorders with INR > 1.5. The lack of specificity and ability to distinguish acute liver failure from previous liver dysfunction disqualifies bilirubin as a single parameter reflecting the complex liver function. Clinical manifestations of sepsis-associated liver dysfunction include hypoxic hepatitis, sepsis-induced cholestasis and dysfunction of protein synthesis manifesting with, e.g., coagulopathies. Detoxifying liver dysfunction, which is associated with an increase in serum ammonia concentration, manifesting with e.g., confusion, loss of consciousness and hepatic encephalopathy, may be disguised by analgosedation used in the intensive care unit. To determine a liver dysfunction in a critically ill patient, the concept of shock liver may be used. It is a complex syndrome of hemodynamic, cellular, molecular and immunologic changes leading to severe liver hypoxia. In clinical practice, there is no standardized diagnostic panel that would allow for an early, clear diagnosis of acute liver dysfunction, and there is no therapeutic panel enabling the full restoration of damaged liver function. The aim of the article is to present the pathophysiology and clinical manifestations of sepsis-associated liver dysfunction.

In the observed period of time, the incidence of CA-UTI was higher than in the INICC (2014) report and the NHSN/CDC (2012) report. Analysis of compliance with a "Urinary Catheter Bundle" to prevent UTI shows low implementation of preventative methods with the INICC protocol.

Serum procalcitonin (PCT) is a sensitive biomarker used for the diagnosis of infection and sepsis. PCT has also some toxic effects. It is not a proinflammatory stimulus, but may augment the inflammatory processes. High levels of PCT in sepsis may lead to hepatocyte necrosis and, as a result, to liver failure. The pathomechanism of the toxic effect of PCT is still unknown. The influence of liver function on PCT levels has not been studied yet. It is not sure whether the liver dysfunction affects the diagnostic and prognostic value of serum PCT levels. In patients with acute liver failure, the usefulness of PCT-level determination remains controversial. Recent studies have shown a potential diagnostic benefit of PCT as a marker of infection in chronic liver diseases. In both groups there is still no consensus on the optimal cut-off value of PCT levels in order to exclude infection. In patients with liver disease, the serum PCT levels should be interpreted with caution, taking into consideration other factors affecting the PCT threshold.

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