Hemodynamics and metabolic studies on septic shock in patients with acute liver failure

被引:19
作者
Tsai, Ming-Hung [2 ]
Chen, Yung-Chang [3 ]
Lien, Jau-Min [2 ]
Tian, Ya-Chung [3 ]
Peng, Yun-shing [4 ]
Fang, Ji-Tseng [3 ]
Yang, Chun [2 ]
Tang, Jui-Hsiang [2 ]
Chu, Yun-Yi [2 ]
Chen, Pang-Chi [2 ]
Wu, Cheng-Shyong [1 ]
机构
[1] Chang Gung Univ, Chang Gung Mem Hosp, Div Gastroenterol, Pu Tz City 613, Chia Yi, Taiwan
[2] Chang Gung Univ, Chang Gung Mem Hosp, Div Gastroenterol, Taipei 105, Taiwan
[3] Chang Gung Univ, Chang Gung Mem Hosp, Div Crit Care Nephrol, Taipei 105, Taiwan
[4] Chang Gung Mem Hosp, Dept Internal Med, Chiayi 613, Taiwan
关键词
Hemodynamics; Tissue oxygenation; Septic shock; Acute liver Failure;
D O I
10.1016/j.jcrc.2008.04.006
中图分类号
R4 [临床医学];
学科分类号
1002 [临床医学]; 100602 [中西医结合临床];
摘要
Backgrounds: Acute liver failure is often accompanied by hyperdynamic Circulation, which is also a characteristic of septic shock. Pre-existing acute liver failure may worsen the hemodynamic impairment and prognosis in sepsis. Aims: To evaluate the hemodynamic and metabolic characteristics and clinical outcomes of septic shock in patients with acute liver failure. Methods: Twenty patients with acute liver failure and 19 patients Without preexisting liver disease were evaluated. Systemic hemodynamics, arterial and mixed vein blood gases, arterial lactate levels, plasma renin activity, and plasma aldosterone levels were checked during the early phase of septic shock. Results: In acute liver failure group, cardiac index (4.92 +/- 1.13 vs 3.69 +/- 11.06 L/min per square meter, P < .001) and oxygen delivery (604.7 +/- 139.7 vs 485.4 +/- 137.3 mL/min per square meter, P = .011) were significantly higher than those without preexisting liver diseases, while systemic vascular resistance index (1041.2 +/- 503.3 vs 1409 +/- 505.25 dyne.s/cm(5).m(2)), oxygen consumption (119.1 +/- 29.2 vs 162.4 +/- 49.4 mL/min per square meter) and oxygen extraction ratio (20% +/- 6% vs. 32% +/- 8%) were significantly higher in the latter group. Furthermore, the patients with acute liver failure had higher arterial lactate (P = .026), plasma renin activity (P = .03), plasma aldosterone levels (P < .001), and intensive care unit as well as hospital mortality rates (P = .005, and 0.02 respectively). Conclusions: In patients With acute liver failure, septic shock was characterized by all accentuated hyperdynamic circulation. hyperlactatemia and all augmented renin-angiotensin-aldosterone system activity. Pre-existing liver failure has a significant impact oil the disease severity of septic shock and portends a grave prognosis. (c) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:468 / 472
页数:5
相关论文
共 27 条
[1]
BLOOD LACTATE LEVELS ARE SUPERIOR TO OXYGEN-DERIVED VARIABLES IN PREDICTING OUTCOME IN HUMAN SEPTIC SHOCK [J].
BAKKER, J ;
COFFERNILS, M ;
LEON, M ;
GRIS, P ;
VINCENT, JL .
CHEST, 1991, 99 (04) :956-962
[2]
BEUTLER B, 2001, LIVER BIOL PATHOBIOL, P581
[3]
DEFINITIONS FOR SEPSIS AND ORGAN FAILURE AND GUIDELINES FOR THE USE OF INNOVATIVE THERAPIES IN SEPSIS [J].
BONE, RC ;
BALK, RA ;
CERRA, FB ;
DELLINGER, RP ;
FEIN, AM ;
KNAUS, WA ;
SCHEIN, RMH ;
SIBBALD, WJ .
CHEST, 1992, 101 (06) :1644-1655
[4]
Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock [J].
Dellinger, RP ;
Carlet, JM ;
Masur, H ;
Gerlach, H ;
Calandra, T ;
Cohen, J ;
Gea-Banacloche, J ;
Keh, D ;
Marshall, JC ;
Parker, MM ;
Ramsay, G ;
Zimmerman, JL ;
Vincent, JL ;
Levy, MM .
CRITICAL CARE MEDICINE, 2004, 32 (03) :858-873
[5]
Circulatory, respiratory, cerebral, and renal derangements in acute liver failure: Pathophysiology and management [J].
Ellis, A ;
Wendon, J .
SEMINARS IN LIVER DISEASE, 1996, 16 (04) :379-388
[6]
Cytopathic hypoxia - Mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis [J].
Fink, MP .
CRITICAL CARE CLINICS, 2001, 17 (01) :219-+
[7]
GANZ NM, 1999, MANUAL CLIN PROBLEMS, P21
[8]
GROSZMANN RJ, 2001, LIVER BIOL PATHOBIOL, P679
[9]
The sympathetic nervous system in liver disease [J].
Henriksen, JH ;
Moller, S ;
Ring-Larsen, H ;
Christensen, NJ .
JOURNAL OF HEPATOLOGY, 1998, 29 (02) :328-341
[10]
Henriksen JH, 1998, ITAL J GASTROENTEROL, V30, P320