Research Spotlight

Caruso, J. P., S. Griffin, T. Y. El Ahmadieh, N. M. Bedros, J. Hoeft, J. F. Urquiaga, M. N. Pernik, K. Hoes, A. R. Patel, R. H. Funk, M. T. Davies, A. Z. Vance, O. Adogwa, S. L. Barnett, C. A. Bagley, H. H. Batjer, J. Coppens, N. El Tecle and S. G. Aoun (2021). “Surgical Site Infection After Autologous Cranioplasty for Decompressive Craniectomy in Traumatic Brain Injury: A Retrospective Review of Two Level 1 Trauma Centers.” J Craniofac Surg 32(8): 2728-2731.

Full text of this article.

OBJECT: Surgical site infection (SSI) after cranioplasty can result in unnecessary morbidity. This analysis was designed to determine the risk factors of SSI after cranioplasty in patients who received a decompressive craniectomy with the autologous bone for traumatic brain injury (TBI). METHODS: A retrospective review was performed at two level 1 academic trauma centers for adult patients who underwent autologous cranioplasty after prior decompressive craniectomy for TBI. Demographic and procedural variables were collected and analyzed for associations with an increased incidence of surgical site infection with two-sample independent t tests and Mann Whitney U tests, and with a Bonferroni correction applied in cases of multiple comparisons. Statistical significance was reported with a P value of < 0.05. RESULTS: A total of 71 patients were identified. The mean interval from craniectomy to cranioplasty was 99 days (7-283), and 3 patients developed SSIs after cranioplasty (4.2%). Postoperative drain placement (P > 0.08) and administration of intrawound vancomycin powder (P = 0.99) were not predictive of infection risk. However, a trend was observed suggesting that administration of prophylactic preoperative IV vancomycin is associated with a reduced infection rate. CONCLUSIONS: The SSI rate after autologous cranioplasty in TBI patients is lower than previously reported for heterogeneous groups and indications, and the infection risk is comparable to other elective neurosurgical procedures. As such, the authors recommend attempting to preserve native skull and perform autologous cranioplasty in this population whenever possible.

Shankar, N., A. Ramani, C. Griffin, U. Agbim, D. Kim, A. Ahmed and S. K. Asrani (2021). “Extrahepatic causes of death in cirrhosis compared to other chronic conditions in the United States, 1999-2017.” Ann Hepatol: 100565.

Full text of this article.

INTRODUCTION AND OBJECTIVES: Cirrhosis- related mortality is underestimated and is increasing; extrahepatic factors may contribute. We examined trends in cirrhosis mortality from 1999-2017 in the United States attributed to liver-related (varices, peritonitis, hepatorenal syndrome, hepatic encephalopathy, hepatocellular carcinoma sepsis) or extrahepatic (cardiovascular disease, influenza and pneumonia, diabetes, malignancy) causes, and compared mortality trends with congestive heart failure (CHF) and chronic obstructive pulmonary disease (COPD) populations. MATERIALS AND METHODS: A national mortality database was used. Changes in age-standardized mortality over time were determined by joinpoint analysis. Average annual percentage change (AAPC) was estimated. RESULTS: Cirrhosis cohort: From 1999-2017, both liver-related (AAPC 1.3%; 95% confidence interval [CI] 0.7-1.9) and extrahepatic mortality (AAPC 1.0%; 95% CI 0.7-1.2) increased. Cirrhosis vs other chronic disease cohorts: changes in all-cause mortality were higher in cirrhosis (AAPC 1.0%; 95% CI 0.7-1.4) than CHF (AAPC 0.1%; 95% CI -0.5- 0.8) or COPD (AAPC -0.4%; 95% CI -0.6- -0.2). Sepsis mortality was highest in cirrhosis (AAPC 3.6%, 95% 3.2- 4.1) compared to CHF (AAPC 0.6%, 95% CI -0.5- 1.7) or COPD (AAPC 0.8%, 95% CI 0.5- 1.2). Cardiovascular mortality increased in cirrhosis (AAPC 1.3%, 95% CI 1.1- 1.5), declined in CHF (AAPC -2.0%, 95% CI -5.3- 1.3) and remained unchanged in COPD (AAPC 0.1%, 95% CI -0.2- 0.4). Extrahepatic mortality was higher among women, rural populations, and individuals >65 years with cirrhosis. CONCLUSIONS: Extrahepatic causes of death are important drivers of mortality and differentially impact cirrhosis compared to other chronic diseases.

Griffin, C., U. Agbim, A. Ramani, N. Shankar, F. Kanwal and S. K. Asrani (2021). “Underestimation of cirrhosis related mortality in the Medicare eligible population, 1999-2018.” Clin Gastroenterol Hepatol Oct 30;S1542-3565(21)01149-6. [Epub ahead of print].

Full text of this article.

The burden of cirrhosis may be increasing, especially among the elderly. A recent updated definition of cirrhosis has a >90% positive predictive value (PPV) for identifying cirrhosis and cirrhosis related complications. We hypothesized that cirrhosis-related mortality is underestimated, and that the elderly are disproportionally impacted. In this study, we aimed to 1) examine trends in liver related mortality using this updated definition among the elderly and 2) identify changes by relevant subsets of gender, race and rurality. [No abstract; excerpt from article].

Asrani, S. K., N. Shankar, B. da Graca, M. K. Nadim and A. Cardenas (2021). “Role of novel kidney biomarkers in patients with cirrhosis and after liver transplantation.” Liver Transpl Oct 29. [Epub ahead of print].

Full text of this article.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are important drivers of morbidity and mortality in patients with cirrhosis before and after liver transplantation (LT). In this review, we examine the role of novel kidney biomarkers for early recognition of kidney injury. Studies are limited by lack of reference standards, heterogeneous definitions of outcomes and biomarker cutoffs, and inconsistent diagnostic performance. Overall, a change in biomarker is more relevant than an absolute cutoff. CIRRHOSIS: Cystatin C and urinary neutrophil gelatinase-associated lipocalin (NGAL) are the most studied candidate biomarkers and identify AKI or progression of AKI earlier than serum creatinine (sCr). Kidney injury molecule 1 and liver-type fatty acid binding protein (L-FABP) also show potential. NGAL and IL-18 may play a role in differentiating acute tubular necrosis from other forms of AKI. Combining novel biomarkers with the Model for End-Stage Liver Disease (MELD) score may assist prognosis. Persistent elevations in select markers (e.g., NGAL) can portend irreversible injury. TRANSPLANT: Several pretransplant markers (including sCr) predict posttransplant kidney dysfunction. Pretransplant assessment of clinical factors (e.g., age, diabetes) and novel markers (osteopontin and TIMP1) may predict renal kidney recovery after LT. Intraoperative changes in biomarkers predict early post-LT AKI. Prediction of CKD remains difficult, although a combination of biomarkers (e.g., beta 2 microglobulin, CD40) are promising. Novel biomarkers have yet to replace sCr in guideline-based evaluation and management of kidney dysfunction in patients with cirrhosis. We propose a theoretical framework for practical incorporation of these biomarkers that considers patient characteristics (risk for irreversible injury), markers of functional and structural change, and assessment of the AKI-CKD continuum to identify patients at highest risk for progressive kidney disease before and after LT.

Asrani, S. K. and J. Levitsky (2021). “Mission accomplished? Early data from the simultaneous liver-kidney transplantation allocation policy.” Am J Transplant 21(11): 3513-3515.

Full text of this article.

This editorial reviews Wilk et al.’s article (page 3593-3607) that reports the initial data following implementation of the 2017 OPTN simultaneous liver-kidney transplantation policy, citing both accomplishments to date and remaining gaps need related to policy success, organ allocation, and transplant patient outcomes.