Liver Transplant Intensive Care Unit Research Articles

Role of EEG in Predicting Outcome of Hepatic Encephalopathy Patients

ABSTRACT Introduction: A retrospective analysis of 151 patients with hepatic encephalopathy (HE) who were admitted to the liver intensive care unit (LICU) and liver transplant intensive care unit (TICU) and underwent electroencephalographic (EEG) testing was performed. We describe a method of grading the EEGs of patients with HE and predicting their subsequent outcomes. Methods: All liver failure patients with HE who underwent routine EEG testing in the LICU or TICU between October 1, 2018 and March 31, 2019, at the Institute of Liver and Biliary Sciences (ILBS) were enrolled in this analysis. The data was analyzed using Statistical Package for the Social Sciences (SPSS). The patients were divided into four grades of HE based on established EEG criteria (HE-EEG). Results: One hundred fifty-one patients [127 Male (84%), 24 Female (16%)] with HE who underwent EEG testing were enrolled. Ages ranged from 3 to 74 years, with a mean age of 48.34 years and median interquartile range (IQR) of 49 years (38–60 years). Ninety-five patients (62.9%) had grade 1 and 2 hepatic encephalopathy, with a statistically significant, worse outcome seen in grades 3 and 4 HE patients. Seizures were seen in 30 (20.1%) of HE patients. Fifteen of 30 patients with seizures (50%) were in the ethanol and nonalcoholic steatohepatitis (NASH) groups. Forty-four of 59 (74.6%) MRIs and 35 of 60 (58.3%) CTs demonstrated some type of brain abnormality in these patients. Imaging abnormalities and the presence of seizures did not contribute to a statistically worse outcome. Conclusion: EEG has an important role in predicting the outcome and prognosis in HE. Patients with grade 3 or 4 HE-EEG, or with progressive worsening of HE-EEG grading were associated with the highest mortality rates.

Minimizing central line–associated bloodstream infections in a high-acuity liver transplant intensive care unit

Increases in liver transplant patient perioperative acuity have resulted in frail immunosuppressed patients at elevated risk for nosocomial infections. Avoiding central line-associated bloodstream infections (CLABSIs) is paramount to facilitate transplantation and post-transplant recovery. In 2015, our liver transplant intensive care unit (ICU) CLABSIs accounted for more than 25% of all CLABSI at our institution. We therefore undertook a multidisciplinary collaborative among clinical epidemiology, nursing, transplant surgery, and critical care to eliminate CLABSI events. From 2014-2016, using Lean methodology and plan-do-study-act (PDSA) cycles, 14 interventions were implemented in the liver transplant ICU. Interventions were aimed at infection prevention, care standardization, and team-based monitoring. Implementation used quality improvement methodology including audit and feedback, education, standardization, multidisciplinary stakeholder involvement, and PDSA cycles. Process measures were monitored and audited. CLABSI rates per 1,000 central venous catheter (CVC) days were tracked by clinical epidemiology. During the intervention, 901 CVC catheter audits were completed. Improvements were seen on all process measures, and complete compliance increased from 25%-67%. CLABSI infection rates dropped from 4.2 to 1.8 in 1,000 CVC days, with an average of less than 1 CLABSI per month. This marked a 61.2% annual reduction, which correlated with an estimated $935,000 annual savings. Concerted ongoing multidisciplinary collaboratives are essential to minimize CLABSI and optimize value and quality in a challenging, high-acuity patient population.

Eliminating Central Line Associated Blood Stream Infections in a High Acuity Liver Transplant Intensive Care Unit

Eliminating Central Line Associated Blood Stream Infections in a High Acuity Liver Transplant Intensive Care Unit

Adrenal function in cirrhosis: The pendulum swings

Adrenal insufficiency (AI) in critically ill patients is a well recognized phenomenon.1 AI may be associated with structural damage to adrenal gland or hypothalamus or resistance to the biological effects of circulating cortisol. The pathophysiological mechanisms of AI in critically ill patients are endotoxemia, increased levels of resultant proinflammatory mediators, decreased levels of apolipoprotein A and high density lipoprotein.1 The same pathophysiological mechanisms are prevalent in patients with liver cirrhosis; hence the term “hepatoadrenal syndrome” was coined in 2005 for AI in patients with liver cirrhosis observed in a liver transplant intensive care unit.2 In a cohort study of 340 patients with liver disease (patients with fulminant liver failure [FHF], chronic liver disease patients who had undergone transplant in the past) AI was diagnosed in 72%. Since the first report, there have been multiple publications on AI in liver diseases, and a recently published systematic review emphasized some major limitations of this entity.3 First, there is no consensus on appropriate tests and normal values to assess the adrenal function in patients with liver disease. Second (and partly as a result of the first point), there is not yet a consensus definition of AI for patients with liver disease. Third, the frequency of AI may vary between different categories of patients, those with fulminant hepatic failure (FHF), critically ill patients with cirrhosis, patients with stable cirrhosis, and those who have received liver transplant. Thus, reported incidence rates of AI in patients with FHF are 33–62%, critically ill patients with cirrhosis 51–66%, patients with stable cirrhosis 9–64% and patients with liver transplant 61–92%. Unfortunately these studies did not adopt a uniform definition of AI. In addition, four studies reported the use of hydrocortisone to treat AI in FHF, acute on chronic liver failure and cirrhotic patients with septic shock. In none of the studies were survival benefits demonstrated.3 In this issue of the Journal, Thevenot et al.4 report high serum levels of free cortisol (SFC) in patients of cirrhosis who were hemodynamically stable. Those with Child–Pugh Class C had higher basal SFC levels than less severe Child–Pugh Class A and B cases. One year non-transplant mortality was higher in patients with high SFC (more than 79 nmol/L). AI based on serum total cortisol (STC) ranged between 7.4% (T0 STC > 139 nmol/L and 49% (change in STC < 250 nmol/L). The authors conclude that their findings are contrary to the “hepatoadrenal syndrome” theory. When we take a close look all the publications on AI in patients with critical illness and liver cirrhosis, these findings are not surprising. Annane et al.12 reported a three level prognostic classification in septic shock based on serum cortisol levels and cortisol response to corticotrophin. High serum total cortisol level was associated with high mortality rate similar to untreated patients with low cortisol levels. Marik et al.2 also reported high mortality rates in patients with high STC levels similar to patients with adrenal failure; they suggested that STC be performed as a marker of disease severity and poor prognosis. Similarly, STC levels and free cortisol levels were shown to vary widely in stable patients with cirrhosis by Tan et al.13 and Fede et al.14 This suggests patients with stable cirrhosis are in a proinflammatory state leading to increased SFC levels, while during further decompensation there may be exhaustion of the adrenal response to stress leading to AI. In summary, adrenal function in patients with cirrhosis needs to be evaluated with appropriate tests, and consensus on normal values and most appropriate diagnostic indices of adrenal function in cirrhosis are now needed. Further studies on adrenal function and insufficiency during the various stages and complications of liver cirrhosis, including detailed analyses of serial changes during longitudinal follow up would be a valuable initiative in this field. Only when these issues are fully canvassed can we know whether AI is a factor contributing to mortality in cirrhosis, and whether therapeutic intervention with corticosteroid replacement has any role in treatment of patients with advanced cirrhosis. Meanwhile, the pendulum will keep swinging!

PTU-063 Effect of intra-operative methylprednisolone on post liver transplant intensive care unit course: further evidence for the existence of hepato-adrenal syndrome?: Abstract PTU-063

<h3>Introduction</h3> Adrenal insufficiency is associated with increased fluid and vasopressor requirements in liver failure and treatment with hydrocortisone improves survival in cirrhotic patients with septic shock.1 Previous data from our unit suggest a high incidence of adrenal insufficiency in patients undergoing liver transplant (LT).2 Adrenal insufficiency appears to be more common in liver transplant programs that use steroid free immunosuppressive regimens but the effect of intraoperative corticosteroids on the outcome of liver transplantation has never been assessed.3 <h3>Methods</h3> We conducted a retrospective analysis of prospectively collected data from 90 consecutive patients undergoing first elective LT, before (Group 1 n=45) and after (Group 2-n=45) the administration of 1000 mg methylprednisalone in the anhepatic phase became standard practise. No other changes to LT treatment protocols were made during the study period. Baseline demographic data and post operative requirements for fluids (12 h and total ITU crystalloid and colloid requirement), vasopressors, renal replacement therapy, ventilation and total stay on the intensive care unit (ITU) were compared between groups. <h3>Results</h3> Indication, MELD score and age at time of LT were not significantly different between groups. There were significantly reduced requirements for fluid, vasopressors, renal replacement therapy, invasive ventilation and ITU stay in group 2 compared with group 1. <h3>Conclusion</h3> Compared to patients undergoing LT in a steroid free regimen, the adminstration of intrapoerative methylprednisolone to patients undergoing LT results in improved post operative haemodynamics and the need for organ support. This finding supports the notion that the common finding of adrenal insufficiency in patients with cirrhosis has clinical importance and that corticosteroid replacement can improve outcome.

The hepatoadrenal syndrome: A common yet unrecognized clinical condition*

Adrenal failure is common in critically ill patients, particularly those with sepsis. As liver failure and sepsis are both associated with increased circulating levels of endotoxin and proinflammatory mediators and reduced levels of apoprotein-1/high-density lipoprotein, we postulated that adrenal failure may be common in patients with liver disease. Clinical study. Liver transplant intensive care unit. The study cohort included 340 patients with liver disease. Based on preliminary observational data, all patients admitted to our 28-bed liver transplant intensive care unit (LTICU) undergo adrenal function testing. An honest broker system was used to extract clinical, hemodynamic, medication, and laboratory data on patients admitted to the LTICU from March 2002 to March 2004. A random (stress) cortisol level <20 microg/dL in a highly stressed patient (respiratory failure, hypotension) was used to diagnose adrenal insufficiency. In all other patients, a random cortisol level <15 microg/dL or a 30-min level <20 microg/dL post-low-dose (1 microg) cosyntropin was considered diagnostic of adrenal insufficiency. Patients were grouped as follows: a) chronic liver failure; b) fulminant hepatic failure; c) patients immediately status post-orthotopic liver transplantation receiving a steroid-free protocol of immunosuppression; and d) patients status post-remote liver transplant (>/=6 months). The decision to treat patients with stress doses of hydrocortisone was at the discretion of the treating intensivist and transplant surgeon. Two-hundred and forty-five (72%) patients met our criteria for adrenal insufficiency (the hepatoadrenal syndrome). Eight (33%) patients with fulminant hepatic failure, 97 (66%) patients with chronic liver disease, 31(61%) patients with a remote history of liver transplantation, and 109 (92%) patients who had undergone liver transplantation under steroid-free immunosuppression were diagnosed with adrenal insufficiency. The high-density lipoprotein level at the time of adrenal testing was the only variable predictive of adrenal insufficiency (p < .0001). In vasopressor-dependent patients with adrenal insufficiency, treatment with hydrocortisone was associated with a significant reduction (p = .02) in the dose of norepinephrine at 24 hrs, whereas the dose of norepinephrine was significantly higher (p = .04) in those patients with adrenal failure not treated with hydrocortisone. In vasopressor-dependent patients without adrenal insufficiency, treatment with hydrocortisone did not affect vasopressor dose at 24 hrs. One hundred and forty-one patients (26.4%) died during their hospitalization. The baseline serum cortisol was 18.8 +/- 16.2 microg/dL in the nonsurvivors compared with 13.0 +/- 11.8 microg/dL in the survivors (p < .001). Of those patients with adrenal failure who were treated with glucocorticoids, the mortality rate was 26% compared with 46% (p = .002) in those who were not treated. In those patients receiving vasopressor agents at the time of adrenal testing, the baseline cortisol was 10.0 +/- 4.8 microg/dL in those with adrenal insufficiency compared with 35.6 +/- 21.2 microg/dL in those with normal adrenal function. Vasopressor-dependent patients who did not have adrenal failure had a mortality rate of 75%. Patients with liver failure and patients post-liver transplantation have an exceedingly high incidence of adrenal failure, which may be pathophysiologically related to low levels of high-density lipoprotein. Treatment of patients with adrenal failure may improve outcome. High baseline serum cortisol levels may be a maker of disease severity and portend a poor prognosis.

Effects of continuous lateral rotation therapy on pulmonary complications in liver transplant patients

When liver transplant candidates and recipients suffer from pulmonary complications of immobility, the results can be life-threatening. Continuous lateral rotation therapy has been reported to decrease complications of immobility. To determine whether continuous lateral rotation therapy decreases the duration of mechanical ventilation, intensive care unit length of stay, incidence or resolution of atelectasis, incidence or onset time of lower respiratory tract infection and pneumonia. Sixty-nine subjects admitted to a liver transplant intensive care unit at a university teaching hospital were randomly assigned to continuous lateral rotation therapy or a stationary bed. All subjects were mechanically ventilated for 24 hours and had a Glasgow Coma Scale score of 11 or less upon admission to the study. Subjects were followed until out of bed, unable to rotate for 3 consecutive days, or transferred from the intensive care unit. Data and chest roentgenogram results were collected on admission and daily during the study. Sputum culture results were obtained if available as part of normal patient care. Incidence of lower respiratory tract infection was significantly lower and length of time to occurrence of lower respiratory tract infection was significantly longer in the continuous lateral rotation therapy group than in the stationary bed group. Although continuous lateral rotation therapy did not affect duration of mechanical ventilation, length of stay, or incidence of atelectasis, it was effective in decreasing the incidence of, and increasing onset time to, lower respiratory tract infection in the liver transplantation population.