Myung Jin Song, Sang Hoon Lee, Ah Young Leem, Song Yee Kim, Kyung Soo Chung, Eun Young Kim, Ji Ye Jung, Young Ae Kang, Young Sam Kim, Joon Chang, Moo Suk Park
Acute Crit Care. 2020;35(2):67-76. Published online May 15, 2020
Background Sepsis-induced cardiomyopathy (SIC) occurs frequently in critically ill patients, but the clinical features and prognostic impact of SIC on sepsis outcome remain controversial. Here, we investigated the predictors and outcomes of SIC.
Methods Patients admitted to a single medical intensive care unit from June 2016 to September 2017 were retrospectively reviewed. SIC was diagnosed by ejection fraction (EF) <50% and ≥10% decrease in baseline EF that recovered within 2 weeks.
Results In total, 342 patients with sepsis met the inclusion criteria, and 49 patients (14.3%) were diagnosed with SIC; the latter were compared with 259 patients whose EF was not deteriorated by sepsis (non-SIC). Low systolic blood pressure and increased left ventricular end-diastolic diameter (LVEDD) were identified as predictors of SIC. SIC and non-SIC patients did not differ significantly in terms of 28-day all-cause mortality (24.5% vs. 26.3%, P=0.936). Acute Physiology and Chronic Health Evaluation II (APACHE II; hazard ratio [HR], 1.10; 95% confidential interval [CI], 1.02 to 1.18; P=0.009) and delta neutrophil index (DNI; HR, 1.02; 95% CI, 1.00 to 1.08; P=0.026) were independent risk factors for 28-day mortality with SIC. DNI, APACHE II, and lactate were identified as risk factors for 28-day mortality in sepsis patients as a whole.
Conclusions SIC was not associated with increased mortality compared to non-SIC. Low systolic blood pressure and increased LVEDD were predictors of SIC. High APACHE II score and elevated DNI, which reflect sepsis severity, predict 28-day all-cause mortality.
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Acute Crit Care. 2020;35(1):24-30. Published online February 29, 2020
Background Hyperbilirubinemia and hypoalbuminemia are frequently appeared and associated with poor prognosis in critically ill patients. We aim to evaluate the association between the bilirubin to albumin ratio and prognosis in intensive care unit (ICU) patients. Methods: This was a retrospective study of 731 patients who were admitted to the medical intensive care unit (MICU) at a tertiary-care center from July 2015 to September 2017. We analyzed the bilirubin to albumin ratio on admission to the MICU, including clinical characteristics and other examinations. Results: The overall 28-day survival of MICU patients was 69.1%. On univariate analysis, Acute Physiology and Chronic Health Evaluation (APACHE) II score (P<0.001), Sequential Organ Failure Assessment score (P<0.001), Simplified Acute Physiology Score II score (P<0.001), Creactive protein (P=0.015), and bilirubin/albumin ratio (P<0.001) were associated with mortality of ICU patients. The receiver operating characteristic curves for ICU patients mortality between bilirubin to albumin ratio and APACHE II score were not statistically significant (P=0.282). On multivariate analysis, higher APACHE II score (hazard ratio [HR], 1.05; 95% CI, 1.03 to 1.06; P<0.001) and bilirubin to albumin ratio (HR, 1.65; 95% CI, 1.23 to 2.20; P=0.001) were independently related to the ICU patient mortality. Conclusions: A higher bilirubin to albumin ratio was related to the unfavorable prognosis and mortality in critically ill patients.
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Background The renin-angiotensin-aldosterone system is closely associated with volume status and vascular tone in septic shock. The present study aimed to assess whether plasma renin activity (PRA) and plasma aldosterone concentration (PAC) measurements compared with conventional severity indicators are associated with mortality in patients with septic shock.
Methods We evaluated 105 patients who were admitted for septic shock. Plasma levels of the biomarkers PRA and PAC, the PAC/PRA ratio, C-reactive protein (CRP) level, and cortisol level on days 1, 3, and 7 were serially measured. During the intensive care unit stay, relevant clinical information and laboratory results were recorded.
Results Patients were divided into two groups according to 28-day mortality: survivors (n = 59) and non-survivors (n = 46). The survivor group showed lower PRA, PAC, Acute Physiologic and Chronic Health Evaluation (APACHE) II score, and Sequential Organ Failure Assessment (SOFA) score than did the non-survivor group (all P < 0.05). The SOFA score was positively correlated with PRA (r = 0.373, P < 0.001) and PAC (r = 0.316, P = 0.001). According to receiver operating characteristic analysis, the areas under the curve of PRA and PAC to predict 28-day mortality were 0.69 (95% confidence interval [CI], 0.58 to 0.79; P = 0.001) and 0.67 (95% CI, 0.56 to 0.77; P = 0.003), respectively, similar to the APACHE II scores and SOFA scores. In particular, the group with PRA value ≥3.5 ng ml-1 h-1 on day 1 showed significantly greater mortality than did the group with PRA value <3.5 ng ml-1 h-1 (log-rank test, P < 0.001). According to multivariate analysis, SOFA score (hazard ratio, 1.11; 95% CI, 1.01 to 1.22), PRA value ≥3.5 ng ml-1 h-1 (hazard ratio, 3.25; 95% CI, 1.60 to 6.60), previous history of cancer (hazard ratio, 3.44; 95% CI, 1.72 to 6.90), and coronary arterial occlusive disease (hazard ratio, 2.99; 95% CI, 1.26 to 7.08) were predictors of 28-day mortality.
Conclusions Elevated PRA is a useful biomarker to stratify the risk of critically ill patients with septic shock and is a prognostic predictor of 28-day mortality.
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Sang Hoon Lee, Byung Hoon Park, Joo Han Song, Song Yee Kim, Kyung Soo Chung, Eun Young Kim, Ji Ye Jung, Young Sam Kim, Se Kyu Kim, Joon Chang, Moo Suk Park
Korean J Crit Care Med. 2016;31(4):324-333. Published online November 30, 2016
Background Despite many ongoing, prospective studies on the topic, sepsis still remains one of the main causes of death in hospital. The hormone insulin-like growth factor 1 (IGF-1) has a similar molecular structure to that of insulin. IGF-1 exerts anabolic effects and plays important roles in both normal physiology and pathologic processes. Previous studies have observed low serum IGF-1 level in patients with critical illnesses. Here, we evaluated changes in IGF-1 level based on survival of septic patients.
Methods We evaluated 140 patients with sepsis and septic shock (21 with sepsis and 119 with septic shock) admitted to the intensive care unit of a university-affiliated hospital in Korea. Serum IGF-1 level was measured on days 0, 1, 3, and 7. Patients with liver disease were excluded from this study. All data were analyzed using SPSS version 20 (SPSS Inc., Chicago, IL, USA).
Results Patients with septic shock had significantly lower serum IGF-1 level on days 1 and 3 than patients without septic shock (p = 0.002 and p = 0.007, respectively). Generally, there was a negative relationship between IGF-1 and serum cortisol levels; however, this relationship was only significant on day 3 (p = 0.029). Furthermore, renin showed significantly negative correlation with IGF-1 on day 3 (p = 0.038). IGF-1 level did not show significant difference between survivors and non-survivors.
Conclusions Our results showed that IGF-1 was associated with septic shock, and that the IGF-1 axis is severely disrupted in septic patients. Additionally, serum cortisol and renin levels were associated with IGF-1 level.
Ji An Hwang, Joo Han Song, Young Seok Lee, Kyung Soo Chung, Song Yee Kim, Eun Young Kim, Ji Ye Jung, Young Ae Kang, Young Sam Kim, Joon Chang, Moo Suk Park
Korean J Crit Care Med. 2016;31(2):140-145. Published online May 31, 2016
Severe hyperammonemia can occur as a result of inherited or acquired liver enzyme defects in the urea cycle, among which ornithine transcarbamylase deficiency (OTCD) is the most common form. We report a very rare case of a 45-year-old Korean male who was admitted to the intensive care unit (ICU) due to severe septic shock with acute respiratory failure caused by Pneumocystis jiroveci pneumonia. During his ICU stay with ventilator care, the patient suffered from marked hyperammonemia (>1,700 μg/dL) with abrupt mental change leading to life-threatening cerebral edema. Despite every effort including continuous renal replacement therapy and use of a molecular adsorbent recirculating system (extracorporeal liver support–albumin dialysis) to lower his serum ammonia level, the patient was not recovered. The lethal hyperammonemia in the patient was later proven to be a manifestation of acquired liver enzyme defect known as OTCD, which is triggered by serious catabolic conditions, such as severe septic shock with acute respiratory failure.
Hemophagocytic lymphohistiocytosis (HLH) is a rare but fatal complication after solid organ transplantation. Acquired forms of HLH are described in association with severe sepsis, autoimmune disorders, malignancy, immune-compromised states, infections, and solid organ transplantation. We experienced a case of hemophagocytic lymphohistiocytosis after bilateral lung transplantation. Leukopenia, thrombocytopenia, and hyperbilirubinemia were noted and became aggravated 50 days after transplantation. Diagnosis of HLH was based on clinical and laboratory findings of splenomegaly, cytopenia, elevated ferritin, elevated interleukin-2 receptor, and hemophagocytosis in bone marrow. Other features such as elevated bilirubin, lactate dehydrogenase, and D-dimer which can be present in HLH were also noted. The patient was immediately treated with etoposide and dexamethasone. Despite aggressive therapy, the patient deteriorated and died. Awareness of the diagnostic criteria of HLH after lung transplantation is important for clinicians.
Hemolytic uremic syndrome (HUS) is defined by the triad of mechanical intravascular hemolytic anemia with schistocytosis, thrombocytopenia and acute renal failure. Pulmonary involvement in HUS is known to be rare. We present the case of a 25-year-old male with diffuse alveolar hemorrhage and myocarditis followed by atypical hemolytic uremic syndrome. In this case, successful treatments included steroid pulse therapy for the fatal alveolar hemorrhage and plasma exchange for the hemolytic uremic syndrome.
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