Indocyanine green elimination rate detects hepatocellular dysfunction early in septic shock and correlates with survival

Citation
S. Kimura et al., Indocyanine green elimination rate detects hepatocellular dysfunction early in septic shock and correlates with survival, CRIT CARE M, 29(6), 2001, pp. 1159-1163
Citations number
34
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
29
Issue
6
Year of publication
2001
Pages
1159 - 1163
Database
ISI
SICI code
0090-3493(200106)29:6<1159:IGERDH>2.0.ZU;2-N
Abstract
Objective: To determine whether indocyanine green clearance is an early ind icator of hepatocellular injury in septic shock and to assess its predictiv e value. Design: Observational study with prospective data collection. Setting: Traumatology and critical care unit in a city hospital, staffed by traumatology and intensive care clinicians. Patients: Twelve patients in septic shock who survived at least 2 months (g roup S) and nine patients who died within 2 wks (group N). Interventions: Routine resuscitation from septic shock (surgery, fluid load ing, and administration of catecholamines and antibiotic drugs). Measurements and Main Results: Pulmonary artery occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, and the indocyanin e green elimination rate constant (K-ICG; or the slope of the loge [indocya nine green concentration] vs, time curve) 3-9 mins after injection were mea sured within 12 hrs of the onset of hypotension, then at 24 hrs, and every 24 hrs thereafter. Alanine aminotransferase and total bilirubin were measur ed on day 0 and day 1. Volume of fluid administered and duration of shock w ere the same in survivors and nonsurvivors. The oxygen consumption index wa s higher in survivors at 12 hrs, but no intergroup difference in pulmonary artery occlusion pressure, cardiac index, or oxygen delivery index was sign ificant at any time point. K-ICG in nonsurvivors was lower than in survivor s both initially and after 24 hrs, and it was subnormal in all patients exc ept one survivor (p < .05). The K-ICG increased between 24 and 120 hrs in 1 1 survivors but progressively decreased and remained below 0.05 in seven no nsunrivors. The remaining two nonsurvivors died within 24 hrs of the initia l measurement of K-ICG, which was >0.05. Alanine aminotransferase and total bilirubin were less sensitive measures of hepatic dysfunction in the first 24 hrs than the K-ICG. Conclusions: The K-ICG can identify reversible liver injury in septic shock , suggesting good prognosis. Either failure to increase the K-ICG within 12 0 hrs or an extremely low K-ICG is a poor prognostic sign.