title: Hemodynamics and metabolic studies on septic shock in patients with acute liver failure.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  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 +/- 1.06 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 an accentuated hyperdynamic circulation, hyperlactatemia and an augmented renin-angiotensin-aldosterone system activity. Pre-existing liver failure has a significant impact on the disease severity of septic shock and portends a grave prognosis.
authors.affiliation: Division of Gastroenterology, Chang Gung Memorial Hospital, Chang Gung University, Taipei 105, Taiwan.
authors.forename: Ming-Hung
authors.initials: MH
authors.lastname: Tsai
authors.forename: Yung-Chang
authors.initials: YC
authors.lastname: Chen
authors.forename: Jau-Min
authors.initials: JM
authors.lastname: Lien
authors.forename: Ya-Chung
authors.initials: YC
authors.lastname: Tian
authors.forename: Yun-Shing
authors.initials: YS
authors.lastname: Peng
authors.forename: Ji-Tseng
authors.initials: JT
authors.lastname: Fang
authors.forename: Chun
authors.initials: C
authors.lastname: Yang
authors.forename: Jui-Hsiang
authors.initials: JH
authors.lastname: Tang
authors.forename: Yun-Yi
authors.initials: YY
authors.lastname: Chu
authors.forename: Pang-Chi
authors.initials: PC
authors.lastname: Chen
authors.forename: Cheng-Shyong
authors.initials: CS
authors.lastname: Wu
mesh_terms: D018806:APACHE; D000450:Aldosterone / Q000097:blood; D001784:Blood Gas Analysis; D005260:Female; D006439:Hemodynamics; D006509:Hepatitis B / Q000150:complications; D017052:Hospital Mortality; D006801:Humans; D019344:Lactic Acid / Q000097:blood; D017114:Liver Failure, Acute / Q000150:complications / Q000378:metabolism* / Q000401:mortality / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism* / Q000401:mortality / Q000503:physiopathology*
chemical_list: D019344:Lactic Acid; D000450:Aldosterone; D012083:Renin