Steve Shaw

Risk factors, sequential organ failure assessment and model for end-stage liver disease scores for predicting short term mortality in cirrhotic patients admitted to intensive care unit.

Background  Prognostic scores in an intensive care unit (ICU) evaluate outcomes, but derive from cohorts containing few cirrhotic patients.

Review article: scoring systems for assessing prognosis in critically ill adult cirrhotics

Cirrhotic patients admitted to intensive care units (ICU) still have poor outcomes. Some current ICU prognostic models [Acute Physiology and Chronic Health Evaluation (APACHE), Organ System Failure (OSF) and Sequential Organ Failure Assessment (SOFA)] were used to stratify cirrhotics into risk categories, but few cirrhotics were included in the original model development. Liver‐specific scores [Child‐Turcotte‐Pugh (CTP) and model for end‐stage liver disease (MELD)] could be useful in this setting.

Prognostic models in cirrhotics admitted to intensive care units better predict outcome when assessed at 48 h after admission

Background and Aim:  The accuracy of prognostic models in critically ill cirrhotics at admission to intensive care units (ICU) may be unreliable. Predictive accuracy could be improved by evaluating changes over time, but this has not been published. The aim of the present study was to assess the performance of prognostic models in cirrhotics at admission (baseline) and at 48 h to predict mortality in the ICU or within 6 weeks after discharge from the ICU.

RIFLE classification as predictive factor of mortality in patients with cirrhosis admitted to intensive care unit

Background and Aim:  To evaluate the association of the Risk, Injury, Failure, Loss and End‐stage renal failure (RIFLE) score on mortality in patients with decompensated cirrhosis admitted to intensive care unit (ICU).

Cirrhotics admitted to intensive care unit: the impact of acute renal failure on mortality.

Background The exact role of renal dysfunction in critically ill cirrhotics admitted to an intensive care unit (ICU) has not been assessed extensively. Aim To evaluate the impact of acute renal failure (ARF) on 6 weeks mortality in cirrhotics admitted to ICU. Patients/methods Three hundred and twelve cirrhotics (182 male, mean age 49.6±11.5 years) were consecutively admitted during the study period. The patients (n=128, 40%) (group 1) with ARF on admission and/or during ICU were compared with the patients whose ICU stay was not complicated with ARF (n=184, 60%) (group 2). At admission, 40 variables were available, whereas Child–Turcotte–Pugh, Model for End-stage Liver Disease, Acute Physiology and Chronic Health Evaluation II, Sequential Organ Failure Assessment and Failure Organ System scores on admission, were evaluated and compared by receiver operating characteristic curves. Results Group 1, compared with group 2 patients, had longer ICU stay (7 vs. 4 days, P=0.04) and required cardiovascular support more frequently with inotropes (90 vs. 75%), (P<0.001). Mortality was significantly higher in group 1, compared with group 2 (91 vs. 47%, P<0.001). At admission, group 1, compared with group 2, had significantly higher Child–Turcotte–Pugh (12 vs. 11), Acute Physiology and Chronic Health Evaluation II (22 vs. 17), Model for End-stage Liver Disease (31 vs. 21), Sequential Organ Failure Assessment (13 vs. 9) and Failure Organ System (3 vs. 2) scores (P<0.001). In group 1, factors independently associated with mortality were: higher FiO2 (P=0.044), bilirubin (P=0.021) and creatinine (P=0.002) on admission. Mortality was not significantly different between those with ARF on admission, and those who developed ARF during ICU stay. Conclusion ARF at admission or during ICU stay is strongly predictive of mortality, which is high, despite supportive therapeutic interventions. Preventive measures are needed to prevent ARF, to improve prognosis.

Comparison of the sequential organ failure assessment score with the King's College Hospital criteria and the model for end‐stage liver disease score for the prognosis of acetaminophen‐induced acute liver failure

Acetaminophen‐induced acute liver failure (ALF) is a complex multiorgan illness. An assessment of the prognosis is essential for the accurate identification of patients for whom survival without liver transplantation (LT) is unlikely. The aims of this study were the comparison of prognostic models [Kings College Hospital (KCH), Model for End‐Stage Liver Disease, Sequential Organ Failure Assessment (SOFA), and Acute Physiology and Chronic Health Evaluation II (APACHE II)] and the identification of independent prognostic indicators of outcome. We evaluated consecutive patients with severe acetaminophen‐induced ALF who were admitted to the intensive care unit. At admission, demographic, clinical, and laboratory parameters were recorded. The discriminative ability of each prognostic score at the baseline was evaluated with the area under the receiver operating characteristic curve (AUC). In addition, using a multiple logistic regression, we assessed independent factors associated with outcome. In all, 125 consecutive patients with acetaminophen‐induced ALF were evaluated: 67 patients (54%) survived with conservative medical management (group 1), and 58 patients (46%) either died without LT (28%) or underwent LT (18%; group 2). Group 1 patients had significantly lower median APACHE II (10 versus 14) and SOFA scores (9 versus 12) than group 2 patients (P < 0.001). The independent indicators associated with death or LT were a longer prothrombin time (P = 0.007), the inspiratory oxygen concentration (P = 0.005), and the lactate level at 12 hours (P < 0.001). The KCH criteria had the highest specificity (83%) but the lowest sensitivity (47%), and the SOFA score had the best discriminative ability (AUC = 0.79). In conclusion, for patients with acetaminophen‐induced ALF, the SOFA score performed better than the other prognostic scores, and this reflected the presence of multiorgan dysfunction. A further evaluation of SOFA with the KCH criteria is warranted. Liver Transpl 18:405–412, 2012.

Continuous renal replacement therapy (CRRT) in patients with liver disease: Is circuit life different?

BACKGROUND/AIMS Clotting of haemofiltration circuits is a major complication of continuous renal replacement therapies (CRRT), yet systemic anticoagulation risks haemorrhage. Traditionally, patients with liver failure are managed with no or minimal anticoagulation, because of abnormal clotting tests and the perceived, increased bleeding risk. METHODS We retrospectively reviewed CRRT circuit life in 50 patients; 3 groups of liver failure patients treated with CRRT (acute liver failure (ALF), acute on chronic liver disease (ACLD) and post-elective liver transplantation (LTx)), with two control groups; systemic sepsis (SS) and haematological malignancy (Haem). RESULTS CCRT circuit life was significantly greater in the Haem group, compared to the others; 24.3+/-23.9h, vs. 11+/-10.5 ALF, 11.6+/-6.6 ACLF, 7.4+/-5.1 LTx and 9.2+/-6.5 SS, p<0.05, with Haem group requiring fewest new CCRT circuits within 48h; 2.4+/-1.0 vs. 4.3+/-1.3 ALF, 4.2+/-2.1 ACLF, 5.3+/-1.5 LTx and 4.6+/-1.5 SS, p<0.05 and least blood transfusions; 1.2+/-1.3 vs. 4.8+/-4.2 ALF, 4.2+/-4.1 ACLF, 2.2+/-2.1 LTx and 3.0+/-1.5 SS. Transmembrane pressures were higher in those CCRT circuits with haemofilter/dialyzer clotting, compared to other causes, such as access dysfunction (123+/-74 vs. 71.8+/-29.3 mm Hg, p=0.009). In those patients in whom anticoagulation was started due to repeated filter clotting, circuit life improved from 5.6+/-3.4 to 19+/-12.7h, p<0.01. CONCLUSION Despite abnormal laboratory coagulation tests and thrombocytopenia, CCRT circuits clot frequently in liver failure patients. Anticoagulation did improve CRRT circuit survival without an obvious increase in bleeding or blood transfusion requirement. Thus anticoagulation should be considered in these patients with repeated circuit clotting.

King's criteria, APACHE II, and SOFA scores in acute liver failure

regardingthecharacteristics and the outcome of acetaminophen-induced acute liverfailure (ALF) in a large cohort of patients in the USA. Interestingly, theyfoundthattheAPACHEIIscoreperformedbetterintermsofpredictingoutcome with a much higher sensitivity and slightly lower specificity,compared with the King’s Hospital criteria. The accompanying editorialhadawordofcautionsuggestingtheKing’scriteriahadnotbeenusedintheclinicalcontextinwhichtheyhadbeenoriginallyderived.Asprophy-lactic use of fresh frozen plasma in the United States was common placethis would have altered the prothrombin time assessment.

Prognostic impact of lactate in acute liver failure

We read with great interest the article by Dhiman et al. regarding the prognostic factors associated with survival in 144 patients with fulminant hepatic failure (FHF) due to acute viral hepatitis. The authors developed a new simple prognostic score, which had a high statistical performance (area under the receiver operating characteristic curve [AUC]: 0.80), followed by the Model for End-Stage Liver Disease (MELD) score (AUC: 0.71), whereas King’s criteria had the lowest ability to discriminate patients who survived from patients who finally died (AUC: 0.67). In the same issue, Yantorno et al. also found that MELD score was superior to King’s and Clichy criteria in 120 patients with FHF of various etiologies. However, we are not sure if their results can be extrapolated in populations with different characteristics, such as patients with FHF due to acetaminophen, which is a very common cause of FHF worldwide. Recently, we published data based on 100 consecutive patients with acetaminophen-induced FHF (41 men, mean age 38 13 years), in which prognostic scores (King’s criteria, the Acute Physiology and Chronic Health Evaluation [APACHE] II, MELD, and Sequential Organ Failure Assessment [SOFA]) and serial arterial blood lactate concentrations at admission, and at 4, 6, and 12 hours postadmission were evaluated. Analyzing our data, we found that MELD score had the lowest performance (AUC: 0.56), compared to the other prognostic scores. Thus, in contrast to the previous studies, MELD score was not useful in our population, which may be explained by the fact that serum bilirubin concentrations are usually low at admission in these patients. Another reason may be the differing end points: survival versus death/liver transplantation and not survival versus death). Our study, similar to Dhiman et al., confirmed that King’s criteria had low sensitivity but with the best specificity in FHF, and it was the first (and to our knowledge, the only one to date), in which SOFA score was evaluated in the setting of FHF. Interestingly, SOFA score had significantly higher discriminative ability (AUC: 0.79) compared to King’s criteria, APACHE II, and MELD (0.65, 0.77, and 0.56, respectively). The predictive accuracy of SOFA score is likely to reflect multiorgan dysfunction, predominant in FHF. Interestingly, based on previous studies, it is known that SOFA score performs well in patients with decompensated cirrhosis. In addition, for the first time, we found that SOFA score at 48 hours postadmission is superior to SOFA score at admission in patients with acute complications of cirrhosis. Dhiman et al. recognized that important survival factors, such as lactate, pH, phosphates, and -fetoprotein, were not assessed in their study, as the data was collected retrospectively over almost 10 years. Currently, serum lactate is considered an established early prognostic marker of survival in patients with FHF. Although the mechanisms of hyperlactemia in severe liver dysfunction are not elucidated precisely, lactate may reflect multiple-organ (for example, hepatic and renal) dysfunction. Thus, not surprisingly, lactate has been found to be an independent factor of mortality in patients with acute complications of cirrhosis. Interestingly, in the latter group of patients, lactate at 48 hours postadmission seems to have a greater impact on survival, compared to lactate at admission. In the setting of FHF, evaluation of lactate at different time points seems to allow more precise assessment of prognosis. For example, similar to Macquillan et al., we found that lactate at 12 hours postadmission had better prognostic accuracy, compared to lactate at admission in acetaminophen-induced FHF. In fact, lactate alone at 12 hours had similar performance to SOFA and better performance than King’s criteria (AUC: 0.76, 0.79, and 0.65, respectively). Importantly, the negative predictive value (NPV), which is low in many prognostic scores in FHF, as acknowledge by Yantorno et al. in their discussion, was higher for lactate at 12 hours (NPV: 0.73), compared to the NPV of the King’s criteria (NPV: 0.65) in our study, and to the NPVs of the new prognostic score and MELD score (NPV: 0.65 and 0.61, respectively) in the study by Dhiman et al.

Is parenteral phosphate replacement in the intensive care unit safe

Hypophosphatemia is well recognized in the intensive care setting, associated with refeeding and continuous forms of renal replacement therapy (CCRT). However, it is unclear as to when and how to administer intravenous phosphate supplementation in the general intensive care setting. There have been recent concerns regarding phosphate administration and development of acute kidney injury. We therefore audited our practice of parenteral phosphate administration. We prospectively audited parenteral phosphate administration (20 mmol) in 58 adult patients in a general intensive care unit in a University tertiary referral center. Fifty‐eight patients were audited; mean age 57.2 ± 2.0 years, 70.7% male. The median duration of the infusion was 310 min (228–417), and 50% of the patients were on CRRT. 63.8% of patients were hypophosphatemic (<0.87 mmol/L) prior to the phosphate infusion, and serum phosphate increased from 0.79 ± 0.02 to 1.07 ± 0.03 mmol/L, P < 0.001. Two patients became hyperphosphatemic (>1.45 mmol/L). There was no correlation between the change in serum phosphate and the pre‐infusion phosphate. Although there were no significant changes in serum urea, creatinine or other electrolytes, arterial ionized calcium fell from 1.15 ± 0.01 to 1.13 ± 0.01 mmol/L, P < 0.01. Although infusion of 20 mmol phosphate did not appear to adversely affect renal function and corrected hypophosphatemia in 67.7% of cases, we found that around 33% of patients who were given parenteral phosphate were not hypophosphatemic, and that the fall in ionized calcium raises the possibility of the formation of calcium‐phosphate complexes and potential for soft tissue calcium deposition.